| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.62444676 |
| Using several carboxy terminal truncated forms of PS 2 , we demonstrated that the hydrophilic amino terminus of PS 2 ( residues 1 to 87 , PS2NT ) was sufficient for interaction with APP . 0.62444676^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Adenovirus class B ( Ad 3 and Ad 7 ) and class C ( Ad 1 , Ad 5 , and Ad 6 ) late r strand mRNA ' s were found to have segmented 5 ' leaders . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The kinetics of cleavage of DNA from Adenovirus Type 1 ( Ad 1 ) , Type 5 ( Ad 5 ) and Type 6 ( Ad 6 ) by restriction endonuclease EcoRI was investigated by quantitative evaluation of the fluorescence from ethidium stained DNA fragments separated on agarose gels . ^^^ The order of the fragment A , B , C , D of Ad 6 DNA obtained after complete cleavage by restriction endonuclease Eco RI was found to be A D C B ; the order of the corresponding fragments A , B , C of Ad 1 and Ad 5 DNA was found to be A C B . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Previous studies of bovine CYP11B1 gene regulation revealed six cis acting elements , Ad 1 , Ad 2 , Ad 3 , Ad 4 , Ad 5 , and Ad 6 , in the 5 ' upstream region of the gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In addition , the combination of a transfected Ad 5 E1A and a beta 1 PKC gene in the same CREF clone results in an enhanced expression of the transformed phenotype in both the absence and presence of TPA . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We tested several new antivirals in vitro , and found that ( S ) HPMPC , ( S ) HPMPA , and 2 ' nor cyclic GMP demonstrated significant serotype dependent inhibitory activity by plaque reduction assay ( ID 50 = 0 . 017 17 . 0 micrograms / ml ) against common clinical ocular isolates and standard adenoviral serotypes ( Ad 1 , Ad 5 , Ad 8 , and Ad 19 ) . ( S ) HPMPC was the least toxic ( CD 50 in A 549 cells = 306 micrograms / ml ) , and ( S ) HPMPC and ( S ) HPMPA had high selectivity indices . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| By analyzing the genetic maps of previously characterized interserotypic recombinants between Ad 2 and Ad 5 and by means of an in vitro proteinase assay using Ad 1 , 2 , 3 , 4 , 5 , 6 , 7 , 9 as the source of enzyme , it was demonstrated that ( 1 ) the enzyme was present in these serotypes and by extension it is likely to be present in all adenoviruses , and ( 2 ) that proteolytic cleavage can take place efficiently even between widely different serotypes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Twenty four percent ( 17 / 72 ) of viruses could not be typed by IEM ; 9 / 17 ( 53 % ) yielded ads [ ad 1 ( 1 ) , ad 2 ( 4 ) , ad 5 ( 1 ) , ad 6 ( 1 ) , ad 7 ( 2 ) ] in routine culture , whereas REA identified the other eight as ad 2 ( 6 ) , ad 1 ( 1 ) , and ad 41 ( 1 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In 13 of 17 peripheral blood lymphocyte samples from adults , 1 of 10 cord blood samples , and seven of seven lymphoblastoid cell lines tested , results were positive for Group C adenovirus DNA ( adenovirus 1 [ Ad 1 ] , Ad 2 , Ad 5 , or Ad 6 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| VA RNAI exists in two forms which differ by two nucleotides : one form is found in Ad 2 and Ad 6 , and the other is found in Ad 1 and Ad 5 . ^^^ There are three sites of variation in Va RNAII , the Ad 1 , Ad 2 , and Ad 5 forms each differing from Ad 6 VA RNAII at one of the positions . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| PGF 2 alpha augmented replication of both oncogenic Ad 12 and latent Ad 1 , Ad 5 serotypes as well as Ad 5 mutants at 32 degrees C and that of mutant ts 18 ( defective in pVI phosphorylation ) but not that of ts 19 ( defective in pX phosphorylation ) at 39 degrees C . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Of 55 isolates altogether , subgenus C ( Ad 1 , Ad 2 , and Ad 5 ) predominated with 42 isolates followed by subgenus B ( Ad 3 and Ad 7 ) with 12 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The most frequently detected type was Ad 2 followed by Ad 1 and Ad 5 . ^^^ Three different genomic variants of both Ad 1 and Ad 5 were discriminated . ^^^ Clearly , one genome type of each serotype predominated over the 7 year period ( Ad 1 D 1 , n = 36 ; Ad 2 D 5 , n = 32 , Ad 5 D 36 , n = 17 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Bovine cytochrome P 450 ( 11 beta ) gene ( CYP11B ) has six different cis acting elements , Ad 1 , Ad 2 , Ad 3 , Ad 4 , Ad 5 , and Ad 6 , in the promoter region . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Five different genome types of Ad 1 , seven genome types of Ad 2 , and three genome types of Ad 5 were identified of , which two , two , and one , respectively , were found to correspond to new DNA variants . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To extend the technique of type specific PCR to other adenovirus serotypes , type specific primers for Ad 1 , Ad 2 , Ad 4 , Ad 5 , Ad 19 and Ad 37 were evaluated . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Ab responses to the Ad 5 vector and to the expressed transgene beta galactosidase ( beta gal ) revealed elevated bronchial and serum IgA and IgG Abs with low neutralization titers . ^^^ Analysis of serum IgG subclass responses showed IgG 1 and IgG2b with lower IgG2a Abs to Ad 5 and IgG2a and IgG2b Ab responses to beta gal . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : Six rabbits per viral isolate were inoculated in each eye after corneal scarification with 1 . 5 10 10 ( 6 ) plaque forming units per eye with one of the following reference or clinical adenovirus isolates : Ad 1 ATCC , Ad 1 Kmetz , Ad 2 ATCC , Ad 2 Wolf , Ad 5 ATCC , Ad 5 McEwen , Ad 6 ATCC , Ad 19 ATCC , and Ad 8 Cray ( five rabbits ) . ^^^ The durations of shedding for Ad 1 ATCC , Ad 1 Kmetz , Ad 2 ATCC , Ad 2 Wolf , and Ad 6 ATCC did not differ statistically from Ad 5 McEwen , whereas Ad 5 ATCC demonstrated a duration of shedding longer than all isolates ( P < 0 . 0001 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The prevalence of neutralizing antibodies in CF children in order of decreasing frequency was 91 . 1 % to Ad 3 , 37 . 5 % to Ad 2 , 27 . 1 % to Ad 1 , 26 . 1 % to Ad 7 , 16 . 7 % to Ad 5 , 8 . 5 % to Ad 4 , and 2 . 0 % to Ad 6 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : The 50 % inhibitory concentration of ketorolac and diclofenac and their respective preservative components were determined for common ocular adenoviral serotypes ( Ad 8 , Ad 19 , Ad 1 , and Ad 5 ) . ^^^ RESULTS : In vitro , neither ketorolac nor diclofenac demonstrated significant inhibitory activity against Ad 1 , Ad 5 , Ad 8 , or Ad 19 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| A collection of 92 epidemiologically unrelated isolates of Ad 1 ( n = 14 ) , Ad 2 ( n = 29 ) , Ad 3 ( n = 19 ) , Ad 5 ( n = 16 ) , and Ad 7 ( n = 14 ) collected in the cities of Belem do Par ( 1 degree S 48 degrees W ) and Rio de Janeiro ( 23 degrees S 43 degrees W ) between 1976 and 1995 from patients with respiratory disease and conjunctivitis were characterized by restriction enzyme analysis of genomic DNA . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| PURPOSE : The goal of the present study was to determine the efficacy of topical 0 . 5 % cidofovir twice daily for 7 days on the replication of multiple adenovirus ( Ad ) serotypes of subgroup C ( Ad 1 , Ad 5 , Ad 6 ) in the New Zealand rabbit ocular model . ^^^ METHODs : In duplicate experiments for each serotype , a total of 20 rabbits ( Ad 5 ) or 16 rabbits each ( Ad 1 and Ad 6 ) were inoculated topically in both eyes , with 1 . 5 10 10 ( 6 ) pfu / eye of the appropriate virus . ^^^ CONCLUSIONS : Topical 0 . 5 % cidofovir twice daily for 7 days demonstrated significant antiviral activity against multiple adenoviral serotypes ( Ad 1 , Ad 5 , and Ad 6 ) in the New Zealand rabbit ocular model . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Four Ad 5 fiber knob mutations , Ser408Glu and Pro409Lys in the AB loop , Tyr477Ala in the DG loop , and Leu485Lys in beta strand F , effectively abolished high affinity binding to CAR , while Ala406Lys and Arg412Asp in the AB loop and Arg481Glu in beta strand E significantly reduced the level of binding . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Examining the babA and babB central regions in 42 H . pylori strains from different geographic locales , we identified five different allele groups of babA ( AD 1 to AD 5 ) and three different allele groups of babB ( BD 1 to BD 3 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| However , only chimeric Ad 5 based constructs in which the hexons from Ad 1 , Ad 2 , Ad 6 , and Ad 12 are incorporated in place of the Ad 5 hexon were successfully rescued into viruses . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To inhibit native receptor binding , we mutated residues in the AB loop of the adenovirus type 5 ( Ad 5 ) fiber . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The common species C adenoviruses ( serotypes Ad 1 , Ad 2 , Ad 5 , and Ad 6 ) infect more than 80 % of the human population early in life . ^^^ DNA from serotypes Ad 1 , Ad 2 , and Ad 5 was detected , while the rarer serotype Ad 6 was not . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Ad 6 showed deletions in motifs 15 17 ( 51 AA ) of the shaft when compared with Ad 1 , Ad 2 , and Ad 5 . ^^^ Phylogenetically , Ad 1 and Ad 6 , including Ad 2 and Ad 5 , formed a subgenus specific cluster , like other serotypes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The isolates included common species B 1 serotypes ( Ad 3 and Ad 7 ) , common species C serotypes ( Ad 1 , Ad 2 , and Ad 5 ) , the less common species B 2 serotype Ad 11 , and three isolates of the rare species B 1 serotype Ad 16 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To determine whether the presenilin 1 ( PS 1 ) , presenilin 2 ( PS 2 ) and amyloid beta protein precursor ( APP ) mutations linked to familial Alzheimer ' s disease ( FAD ) increase the extracellular concentration of amyloid beta protein ( A beta ) ending at A beta 42 ( 43 ) in vivo , we performed a blinded comparison of plasma A beta levels in carriers of these mutations and controls . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the genes encoding amyloid beta precursor protein ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) are known to cause early onset , autosomal dominant Alzheimer ' s disease . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Most early onset forms of Alzheimer ' s disease ( AD ) have been linked to mutations of the presenilin 1 , presenilin 2 or APP genes , located on chromosomes 14 , 1 and 21 , respectively . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Genetic studies have led to the identification of 3 genes , beta amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) , which , when mutated , can cause familial forms of AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To test whether presenilins interfere with APP metabolism , presenilin 2 ( PS 2 ) was coexpressed with APP in mammalian cells . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| It was established that missense mutations in the genes encoding APP , presenilin 1 , and presenilin 2 , all treated APP processing , leading to increased production of A beta 42 . ^^^ On the other hand , many missence mutations in APP gene and other gene , S 182 ( presenilin 1 ) , and STM 2 ( presenilin 2 ) were identified in familial AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| These are related to chromosomes 14 ( presenilin 1 ) , 21 ( beta APP gene ) , 1 ( presenilin 2 ) , 19 ( epsilon 4 alleles ) , and other . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Genetic studies have led to the identification of three genes which , when mutated , cause familial forms of Alzheimer ' s disease ( AD ) : the beta amyloid precursor protein gene ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Genetic causes of Alzheimer ' s disease ( AD ) include mutations in the amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We analyzed the effect of the ApoE genotype in two distinct early onset familial AD groups : families with a mutation in the presenilin 1 gene ( PS 1 ) on chromosome 14 , and families without a mutation detectable in the PS 1 , presenilin 2 ( PS 2 ) , and the amyloid precursor protein ( APP ) gene ( non PS early onset familial AD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The developmental pattern of APP moeities in mouse hypothalamus and in fetal hypothalamic neurons in culture was compared with a presenilin 2 ( PS 2 ) related protein using an antibody developed against the N terminal part of PS 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Using positional cloning , most of the genes which lead to FAD have recently been identified e . g . , the amyloid precursor protein ( APP ) gene on chromosome 21 , presenilin 1 on chromosome 14 and presenilin 2 on chromosome 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We examined mutations of presenilin 1 ( PS 1 ) , presenilin 2 ( PS 2 ) and amyloid precursor protein ( APP ) in 30 Japanese familial Alzheimer ' s disease ( FAD ) and 34 isolated cases of Alzheimer ' s disease ( AD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We hypothesized that in some cases of sporadic AD , a somatic mutation in an embryonic cell committed to neuronal development within the amyloid precursor protein ( APP ) , the presenilin 1 ( PS 1 ) or the presenilin 2 ( PS 2 ) genes ( genes known to be involved in familial AD ) may result in AD phenotype . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Previous data from familial AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein suggest that the long form of Abeta peptide , Abeta 42 , is selectively increased in these circumstances . ^^^ CONCLUSION : Our results differ from the data from AD due to mutations in presenilin 1 and presenilin 2 genes and the amyloid precursor protein and suggest that the APOE epsilon 4 genotype mediates increased Abeta deposition by a mechanism that differs from that found in other genetic causes of AD . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Germ line mutations in three genes have been detected in patients with familial Alzheimer ' s disease ( FAD ) and sporadic , early onset disease : amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 2 ( PS 2 ) is one of three genes [ amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) and PS 2 ] shown to cause familial Alzheimer ' s disease ( FAD ) , and is highly homologous to PS 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| More than 40 missense mutations and a splice site mutation in the presenilin 1 ( PS 1 ) gene , two missense mutations of presenilin 2 ( PS 2 ) , and more than three missense mutations of amyloid precursor protein ( APP ) cosegregate with early onset familial Alzheimer ' s disease ( FAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The second part describes the three genes , amyloid precusor protein ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) genes , which when mutated cause early onset autosomal dominant AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The three causative genes are the amyloid precursor protein ( APP gene ) on chromosome 21 , the presenilin 1 gene on chromosome 14 , and the presenilin 2 gene on chromosome 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Three genes have been identified which , when mutated , cause AD : the Abeta amyloid precursor protein gene ( APP ) , and the presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| These included presenilin 1 , presenilin 2 , and amyloid precursor protein ( APP ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In addition , mutations in the gene presenilin 2 on chromosome 1 and in the amyloid precursor protein gene ( APP on chromosome 21 ) occur in autosomal dominant AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) genes have been identified as the causative genes for early onset familial Alzheimer ' s disease . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In a series of sibpairs with late onset Alzheimer ' s disease , we have examined the segregation of the loci involved in the early onset , autosomal dominant form of the disorder by using flanking microsatellite repeat markers : thus we have used APP PCR 3 and D21S210 to examine the segregation of the amyloid beta precursor protein ( APP ) gene , the markers DI 4S77 and D14S284 to examine the segregation of the presenilin 1 ( PSI ) gene and the markers D1S227 , D1S249 and D1S419 to examine the segregation of presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We then performed a mutational analysis of the genes for amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) , and presenilin 2 ( PSEN 2 ) in 34 families with ADEOAD ascertained in France . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Expression of autosomal dominant mutations in the genes for the amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) in affected patients , cultured cells , or transgenic mice leads to increased production of total A beta or increased production of A beta ending at residue 42 ( A beta 42 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in any one of three genes can cause autosomal dominant , early onset Alzheimer ' s disease : these genes are the amyloid precursor protein ( APP ) gene on chromosome 21 , the presenilin 1 ( PS 1 ) gene on chromosome 14 and the presenilin 2 ( PS 2 ) gene on chromosome 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| At no time point did we observe significant changes in Abeta 40 , APP holoprotein , presenilin 2 , or tubulin . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : The discovery of nonbeta amyloid ( Abeta ) , plaque like deposits composed of a 100 kd protein ( AMY ) in sporadic AD ( SAD ) brains prompted us to determine whether these plaques ( AMY plaques ) also occur in AD due to mutations of the presenilin 1 ( PS 1 ) , presenilin 2 ( PS 2 ) , or the amyloid precursor protein ( APP ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Dominant mutations have been identified , in the beta amyloid precursor protein gene ( APP ) , and in two homologous genes presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| All mutations in the three FAD genes , i . e . , amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) cause an increased production of a longer , more amyloidogenic form of the amyloid peptide corroborating strongly the idea that abnormal processing of APP is central to the pathogenesis . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The beta amyloid precursor protein ( beta APP ) gene ( on chromosome 21 ) , the presenilin 1 ( PS 1 ) gene ( on chromosome 14 ) , and the presenilin 2 ( PS 2 ) gene ( on chromosome 1 ) gene are all associated with early onset AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the genes amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) have been found in early onset familial forms of Alzheimer disease OBJECTIVE : To determine the cause of dementia in a family with early onset illness . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| So far , three genes have been identified in which mutations cause autosomal dominant AD : the amyloid precursor protein ( APP ) gene on chromosome 21 , the presenilin 1 ( PSEN 1 ) gene on chromosome 14 , and the homologous presenilin 2 ( PSEN 2 ) gene on chromosome 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To date , mutations in three genes , beta amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) , have been found to be causally related to familial Alzheimer ' s disease ( AD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 2 mutation does not influence expression and concentration of APP forms in human platelets . ^^^ The aims of this study were to evaluate in platelets of symptomatic and presymptomatic patients carrying the mutation Met239Val in presenilin 2 ( PS 2 ) whether : 1 ) PS 2 and presenilin 3 ( PS 1 ) were expressed in platelets ; 2 ) an altered expression of different APP isoforms mRNAs could be related to the presence of the mutation ; and 3 ) an abnormal pattern of APP forms was associated to the mutation . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Subcellular compartment and molecular subdomain of beta amyloid precursor protein relevant to the Abeta 42 promoting effects of Alzheimer mutant presenilin 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Recently , some Alzheimer associated genes have been found : amyloid precursor protein ( APP ) , apolipoprotein E ( apoE ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Three genes have been identified that cause the less common early onset , familial cases of the disease : the amyloid precursor ( APP ) protein gene on chromosome 21 , the presenilin 1 ( PSEN 1 ) gene on chromosome 14 and the presenilin 2 ( PSEN 2 ) gene on chromosome 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Nearly all mutations in the presenilin 1 ( PSEN 1 ) , presenilin 2 ( PSEN 2 ) , and amyloid beta precursor protein ( APP ) genes lead to early onset Alzheimer disease ( EOAD , onset age at or before 65 years ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Recently , some Alzheimer associated genes have been found : amyloid beta protein precursor ( APP ) , apolipoprotein E ( apoE ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations of three different genes amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , presenilin 2 ( PS 2 ) have been found in early onset autosomal dominant forms of AD , of the human microtubule associated protein tau gene ( MAPT ) in frontotemporal dementia and parkinsonism linked to chromosome 17 ( FTDP 17 ) , of the BRI gene in familial British dementia , of the PI 12 gene in familial encephalopathy with neuroserpin inclusion bodies . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| PSEN 1 and PSEN 2 encode polytopic membrane proteins , termed presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) that play an essential role in intramembranous ( `` gamma secretase ' ' ) proteolysis of selected type 1 membrane proteins , that include Notch 1 and beta amyloid precursor protein ( APP ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here , we report the production of endogenous secreted and intracellular 40 and 42 amino acid Abeta peptides in mouse fibroblasts deficient in presenilin 1 , presenilin 2 or both . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) proteins are necessary for proteolytic cleavage of the amyloid precursor protein ( APP ) within its transmembrane domain . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The autosomal dominant inherited forms of early onset Alzheimer ' s disease are caused by mutations in the genes encoding APP , presenilin 1 ( chromosome 14 ) , and presenilin 2 ( chromosome 1 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 1 ( PS 1 ) , presenilin 2 , and nicastrin form high molecular weight complexes that are necessary for the endoproteolysis of several type 1 transmembrane proteins , including amyloid precursor protein ( APP ) and the Notch receptor , by apparently similar mechanisms . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Over 100 mutations have been identified in three causative genes , i . e . amyloid protein precursor ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) genes , for early onset autosomal dominant familial AD ( FAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 1 ( PS 1 ) and presenilin 2 play a critical role in the gamma secretase processing of amyloid precursor protein ( APP ) and Notch 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : A mutational analysis of the amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) , and presenilin 2 ( PSEN 2 ) genes was performed in 31 probands with probable or definite AD from UK families with an age at onset ( AAO ) < 61 years . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We show first that overexpression of the presenilinase derived maturation product of presenilin 2 ( CTF PS 2 ) increases Abeta recovery , the production of which is almost abolished by a caspase 3 inhibitor and increased by staurosporine . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The final step in A beta generation is the cleavage of the C terminal 99 amino acid residues of the amyloid precursor protein by gamma secretase . gamma Secretase activity is closely linked to the multi transmembrane spanning proteins presenilin 1 and presenilin 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Autosomal dominant forms of familial Alzheimer ' s disease ( FAD ) are caused by mutations of the amyloid precursor protein ( APP ) gene and by mutations of the genes encoding for presenilin 1 or presenilin 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Three genes have been identified as responsible for the rare early onset familial form of the disease : the amyloid precursor protein ( APP ) gene , the presenilin 1 ( PSEN 1 ) gene and the presenilin 2 ( PSEN 2 ) gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To date 3 genes responsible for EOAD have been identified : the amyloid precursor protein gene ( APP ) , presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| MUTATIONS : The more frequent mutations are found in the Presenilin 1 gene ( PS 1 ) , mutations in the amyloid precursor protein ( APP ) are rare and only a few Presenilin 2 gene ( PS 2 ) mutations are reported . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : Autosomal dominant early onset Alzheimer disease is a heterogeneous condition that has been associated with mutations in 3 different genes : the amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) , and presenilin 2 ( PSEN 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Familial Alzheimer ' s disease ( FAD ) accounts for 5 10 % of deaths from Alzheimer ' s disease ( AD ) , and approximately 50 % of these cases have been definitely linked to missense mutations in three genes , encoding the amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here , we have investigated the effect of membrane cholesterol content on gamma secretase activity using Chinese hamster ovary cells stably expressing beta amyloid precursor protein ( APP ) and either wild type or N141I mutant type presenilin 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To investigate the generation of intracellular Abeta , we established human neuroblastoma SH SY5Y cells stably expressing wild type amyloid precursor protein ( APP ) , Swedish mutant APP , APP plus presenilin 1 ( PS 1 ) and presenilin 2 ( PS 2 ; wild type or familial AD associated mutant ) , and quantified intracellular Abeta 40 and Abeta 42 in formic acid extracts by sensitive Western blotting . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To determine the spectrum of mutations in a group consisting of 40 Polish patients with clinically diagnosed familial EOAD and 1 patient with mild cognitive impairment ( MCI ) and family history of AD , we performed a screening for mutations in the presenilin 1 ( PSEN 1 ) , presenilin 2 ( PSEN 2 ) and amyloid precursor protein ( APP ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Autosomal dominant forms of FAD are caused by mutations of the amyloid precursor protein ( APP ) gene and by mutations of the genes encoding for presenilin 1 or presenilin 2 ( PS1 / 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The beta amyloid precursor protein ( APP ) gene ( on chromosome 21 ) , Presenilin 1 ( PS 1 ) gene ( on chromosome 14 ) and Presenilin 2 ( PS 2 ) gene ( on chromosome 1 ) are responsible for autosomal dominant early onset Alzheimer ' s disease ( EOAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| One of the strong pieces of evidence supporting this hypothesis was the identification of pathogenic mutations within APP , presenilin 1 and presenilin 2 genes responsible for familial autosomal dominant AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in presenilin 1 gene ( PSEN 1 ) , located on chromosome 14 , more rarely in amyloid beta protein precursor ( APP ) on chromosome 21 , and presenilin 2 genes ( PSEN 2 ) on chromosome 1 , underlie the pathogenesis of most cases of familial early onset of AD ( EOAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : Early onset familial Alzheimer disease is caused by mutations in the amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) , or presenilin 2 ( PSEN 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| However , this hypothesis is inconsistent with the presence in normal aged human brain of the beta amyloid plaque burden similar to that in AD , and the absence of neurofibrillary pathology and neurodegeneration in mutated APP , presenilin 1 and presenilin 2 transgenic mice that show extensive beta amyloid plaque pathology . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 2 familial Alzheimer ' s disease mutations result in partial loss of function and dramatic changes in Abeta 42 / 40 ratios . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in three genes ( amyloid precursor protein / APP , presenilin 1 , presenilin 2 ) cause early on set familial AD by increasing synthesis of the toxic 42 amino acid species of Abeta ( Abeta 42 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Three genes have been identified which , when mutated , cause Familial Alzheimer disease ( FAD ) : the presenilin 1 ( PS 1 ) , the presenilin 2 ( PS 2 ) and the amyloid precursor protein ( APP ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in beta amyloid precursor protein ( APP ) , presenilin 1 and presenilin 2 associated with familial Alzheimer ' s disease ( FAD ) increase release of Abeta 42 , suggesting that FAD may directly result from increased gamma secretase activity . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Genetic assessment included the analysis of genes involved in AD , such as the genes for amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| DEVELOPMENT : Molecular analysis of families with early onset AD has made it possible to identify mutations in three different genes that are responsible for the disease : the gene encoding for the amyloid precursor protein peptide ( APP ) , and the presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) and presenilin 2 ( PSEN 2 ) genes are associated with early onset familial Alzheimer ' s disease ( EOAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In familial Alzheimer ' s disease , Abeta is excessively produced and deposited because of mutations in the amyloid precursor protein , presenilin 1 , and presenilin 2 genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations of the amyloid precursor protein ( APP ) , presenilin 1 ( PSEN 1 ) , and presenilin 2 ( PSEN 2 ) genes have been identified . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : At least half of all cases of early onset ( < 60 ) familial Alzheimer ' s disease ( FAD ) are caused by any of over 150 mutations in three genes : the amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , and presenilin 2 ( PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Furthermore , mutations in the genes encoding presenilin 1 and presenilin 2 , that cause FAD , also lead to changes in AbetaPP processing and Abeta deposition . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Each PS integrin consists of an alpha subunit , alpha PS 1 or alpha PS 2 , and a beta PS subunit . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We found the mutations , G384A , E280A in two FAD and H163R in one sporadic AD patient , and no N 1411 or M239V mutation in PS 2 gene , and no mutation in exons 16 and 17 in amyloid precursor protein ( APP ) gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| While the pathogenic mutations in the early onset FAD genes , APP , PS 1 , and PS 2 directly cause AD with nearly 100 % penetrance , in a larger subset of AD cases with onset over 60 years ( maximally for onset at 61 65 years ) , inheritance of the APOE 4 allele confers increased risk for AD but is not sufficient to cause the disease . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the transfected cells , PS 1 and PS 2 mutations caused a highly significant increase in A beta 42 secretion in all mutant clones . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid beta protein ( Abeta ) deposition was investigated in the frontal cortex of 6 cases of ( genetically confirmed ) chromosome 1 linked Alzheimer ' s disease ( AD ) ( PS 2 gene mutation ) among the Volga German families using the end specific monoclonal antibodies BA 27 and BC 05 to detect the presence of Abeta 40 and Abeta 42 ( 43 ) , respectively . ^^^ Therefore , mutations in the PS 2 gene , like those in the presenilin 1 ( PS 1 ) and amyloid precursor protein ( APP ) genes , are associated with an initial and preferential deposition of Abeta 42 ( 43 ) within the brain . ^^^ Although the mechanism ( s ) whereby the PS 1 and PS 2 gene mutations operate remains unclear , it seems from the present study that the effect of the PS 2 gene mutation on the brain is much less severe , at least as far as Abeta deposition is concerned , than that of the PS 1 mutation , which seems to confer a much earlier and a much more aggressive development of AD . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutant PS 1 or PS 2 consistently induced a 1 . 4 2 . 5 fold increase ( p < 0 . 001 ) in the relative production of the highly amyloidogenic 42 residue form of amyloid beta protein ( Abeta 42 ) as determined by quantitative immunoprecipitation and by enzyme linked immunosorbent assay . ^^^ In mutant PS 1 and PS 2 cell lines with high increases in Abeta42 / Abetatotal ratios , spontaneous formation of low molecular weight oligomers of Abeta 42 was observed in media , suggesting enhanced Abeta aggregation from the elevation of Abeta 42 . ^^^ We conclude that mutant PS 1 and PS 2 proteins enhance the proteolysis of beta amyloid precursor protein by the gamma secretase cleaving at Abeta residue 42 , thereby promoting amyloidogenesis . . ^^^ To elucidate their pathogenic mechanism , wild type ( wt ) or mutant ( M146L , C410Y ) PS 1 and wt or mutant ( M239V ) PS 2 genes were stably transfected into Chinese hamster ovary cells that overexpress the beta amyloid precursor protein ( APP ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We analyzed the distribution of the PS 1 intronic polymorphism in patients with sporadic AD and in seven familial AD ( FAD ) families carrying pathogenetic mutations in the amyloid precursor protein ( APP ) and Presenilin ( PS 1 and PS 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| AD in these pedigrees can be caused by missense mutations within the recently identified PS 1 ( S 182 ) gene on chromosome 14 ( AD 3 locus ) and the PS 2 ( STM2 / E5 1 ) gene on chromosome 1 , in addition to previously described point mutations of the beta A 4 amyloid protein precursor ( APP ) gene on chromosome 21 ( AD 1 locus ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To gain insights into the significance of presenilins ( PS ) in the pathogenetic mechanisms of early onset familial Alzheimer disease ( FAD ) , we expressed cDNAs for wild type PS 2 and PS 2 with the Volga German ( N141I ) mutation in cultured cells and then examined the metabolism of the transfected proteins and their effect on the C terminal properties of secreted amyloid beta protein ( A beta ) . ^^^ COS 1 cells doubly transfected with cDNAs for N141I mutant PS 2 and human beta amyloid precursor protein ( betaAPP ) or a C terminal fragment thereof , as well as mouse Neuro2a neuroblastoma cells stably transfected with N141I mutant PS 2 alone , secreted 1 . 5 to 10 fold more A beta ending at residues 42 ( or 43 ) [ A beta 42 ( 43 ) ] compared with those expressing the wild type PS 2 . ^^^ These results strongly suggest that the PS 2 mutation ( N141I ) linked to FAD alters the metabolism of A beta / betaAPP to foster the production of the form of A beta that most readily deposits in amyloid plaques . ^^^ Thus , mutant PS 2 may lead to AD by altering the metabolism of A beta / betaAPP . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Of the five remaining families and the other early onset case , none have missense mutations in the PS 1 or PS 2 genes , or in exon 16 and 17 of the APP gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Findings to date suggest an important role of presenilins in beta amyloid ( A beta ) production : in vitro and in vivo studies have shown that presenilin mutations are associated with relatively increased production of the longer , and highly fibrillogenic A beta 42 ( 43 ) peptide , and a marked elevation in the number of A beta 42 immunoreactive plaques in the brains of individuals with familial AD who carry PS 1 and PS 2 mutations . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To elucidate the molecular mechanism of this effect , wild type ( wt ) or mutant PS 1 and PS 2 genes were stably transfected into Chinese hamster ovary cells expressing endogenous or transfected beta amyloid precursor protein ( APP ) . ^^^ By immunoprecipitation / Western blot analysis , APP was consistently found to coimmunoprecipitate with PS 1 or PS 2 proteins . ^^^ Several distinct PS 1 , PS 2 , or APP antibodies precipitated PS APP complexes that were detectable by blotting with either APP or PS antibodies . ^^^ Our results demonstrate that wt and mutant PS 1 and PS 2 proteins form complexes with APP in living cells , strongly supporting the hypothesis that mutant PS interacts with APP in a way that enhances the intramembranous proteolysis of the latter by a gamma secretase cleaving at Abeta42 . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The beta APP gene on chromosome 21 , the PS 1 gene on chromosome 14 , and the PS 2 gene on chromosome 1 have all been characterized as genes in which mutations lead to familial EOAD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Some cases of AD , particularly those of early onset , are familial and inherited as autosomal dominant disorders linked to the presence of mutant genes that encode the amyloid precursor protein ( APP ) or the presenilins ( PS 1 or PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Previously , we have shown that PS 2 , a homolog of PS 1 . regulates apoptosis induced in neurons by trophic withdrawal or Abeta , and in T cells by Fas ligand . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The amyloid beta protein ( Abeta ) 42 levels in the brains of mutant PS 2 transgenic mice were higher than those in wild type PS 2 transgenic mice at the age of 2 , 5 , or 8 months . ^^^ In addition , the Abeta 42 levels appeared to increase steadily in the mutant PS 2 transgenic mouse brains from 2 to 8 months of age , whereas there was only a small increase in wild type transgenic mice between the ages of 5 and 8 months . ^^^ These data show a definite effect of the PS 2 mutation on an age dependent increase of Abeta 42 content in the brain . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Moreover , and in contrast to published reports which documented that PS 1 and PS 2 form stable heteromeric assemblies with the beta amyloid precursor protein ( APP ) , we have failed to provide evidence for physiological complexes between PS 1 and PS 2 holoproteins or their derivatives with APP . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To date , mutations in three genes account for some of them : the amyloid precursor protein ( APP ) and presenilins 1 and 2 ( PS 1 and PS 2 , respectively ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Autosomal dominant familial AD ( FAD ) , linked to mutations in presenilin ( PS 1 and PS 2 ) genes or the amyloid precursor protein ( APP ) gene , shows brain abnormalities ( e . g . , neurofibrillary tangles , deposits of . amyloid A . , and death of subsets of neurons ) similar to those that occur in sporadic AD , the risk of which is enhanced by the presence of one or two copies of apolipoprotein E 4 ( apoE 4 ) alleles . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Inability of truncated forms of PS 2 with familial Alzheimer ' s disease mutation to increase secretion of Abeta 42 . ^^^ Mutations in presenilin ( PS ) 1 or PS 2 genes account for the majority of early onset familial Alzheimer ' s disease , and these mutations have been shown to increase production of species of amyloid beta peptide ( Abeta ) ending at residue 42 , i . e . the most amyloidogenic form of Abeta . ^^^ To gain insight into the molecular mechanisms whereby mutant PS induces overproduction of Abeta 42 , we constructed cDNAs encoding mutant and / or truncated forms of PS 2 and examined the secretion of Abeta 42 from COS or neuro2a cells transfected with these genes . ^^^ Cells expressing full length PS 2 harboring both N141I and M239V mutations in the same polypeptide induced overproduction of Abeta 42 , although the levels of Abeta 42 were comparable with those in cells engineered to express PS 2 with one or the other of these PS 2 mutations . ^^^ In contrast , cells engineered to express partially truncated PS 2 ( eliminating the COOH terminal third of PS 2 while retaining the endoproteolytic NH 2 terminal fragment ) and harboring a N141I mutation , as well as cells expressing COOH terminal fragments of PS 2 , did not overproduce Abeta 42 , and the levels of Abeta 42 were comparable with those in cells that expressed full length , wild type PS 2 or fragments thereof . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Although approximately 50 % of the PS 1 and both PS 2 mutations occur within the N terminal region lacking in the PS 2 deltaexon3 , 4 and PS 2 deltaexon3 , 4 , 8 proteins , expression of these truncated proteins does not affect pathological generation of amyloid beta peptide ( Abeta ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in two familial AD linked genes , presenilins 1 ( PS 1 ) and 2 ( PS 2 ) , selectively increase the production of Abeta 42 in cultured cells and the brains of transgenic mice , and gene deletion of PS 1 shows that it is required for normal gamma secretase cleavage of the beta amyloid precursor protein ( APP ) to generate Abeta . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In early onset familial Alzheimer ' s disease ( AD ) pathogenic mutations have been found in the amyloid precursor protein ( APP ) gene and in the presenilin ( PS ) 1 and PS 2 genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Missense mutations in the genes coding for APP and for the polytopic membrane proteins presenilin ( PS ) 1 and PS 2 have been linked to familial forms of early onset Alzheimer ' s disease . ^^^ When we analyzed APP in COS 7 cells overexpressing PS 2 , we observed proteolytic processing close to the APP carboxyl terminus . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Double labeling immunocytochemistry detected very few neurones with combined immunoreactivity PS 2 and APP , or PS 2 and Tau . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We found that exogenous expression of the PS 1 NTF or PS 2 NTF harboring FAD mutations was insufficient for increased production of amyloidogenic A beta 10 42 peptide and that the overexpressed NTFs had no effect on the accumulation of endogenous presenilin fragments . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Abeta 1 42 formation is favoured by mutations in the two presenilin genes ( PS 1 and PS 2 ) , and by the commonest amyloid precursor protein mutations . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the case of familial AD , defects in at least three different genes ( APP , PS 1 , PS 2 ) leading to indistinguishable pathology are now well defined . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| RESULTS : We showed that transient and stable transfection of CTF PS 1 and CTF PS 2 cDNAs in human cells leads to increased secretion of APP alpha and A beta , the maturation products of beta APP . ^^^ CONCLUSION : Our data establish that the C terminal products of PS 1 and PS 2 maturation exhibit biological activity and in particular control beta APP maturation upstream to alpha and beta / gamma secretase cleavages . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The levels of Alzheimer ' s disease ( AD ) related genes , including beta amyloid precursor protein ( APP ) , presenilin 1 ( PS 1 ) , PS 2 , apoE , tau , c fos , neural cell adhesion molecular 180 ( NCAM 180 ) , TGF beta 1 , IL 1 alpha / beta , IL 6 , TNF alpha / beta , alpha 2 Macroglobulin ( alpha 2M ) , class 2 major histocompatibility antigen la ( MHCII la ) , bcl 2 alpha , glucocorticoid receptor alpha ( GR alpha ) and mineralocorticoid receptor ( MR ) mRNAs were determined by reverse transcription polymerase chain reaction ( RT PCR ) in the hippocampus and cerebral cortex of senescence accelerated mouse ( SAM ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Caspases degrade amyloid precursor protein ( APP ) , presenilins ( PS 1 , PS 2 ) , tau , and huntingtin , raising questions on their role in neurodegeneration . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| All the PS 1 and PS 2 mutations assessed in this series led to enhanced deposition of total Abeta and Abeta ( 10 42 / 43 ) but not Abeta ( 10 40 ) senile plaques in the superior temporal sulcus when compared with brains from sporadic Alzheimer ' s disease patients . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Although Alzheimer ' s disease associated mutations in the homologous presenilin ( PS 2 ) gene elevate amyloid beta peptide ( Abeta 42 ) production like PS 1 mutations , here we demonstrate that a gene ablation of PS 2 ( unlike that of PS 1 ) in mice does not result in a severe phenotype resembling that of Notch ablated animals . ^^^ The reduced gamma secretase activity results in the almost complete inhibition of Abeta and p 3 production in cells stably expressing PS 2 D366A , whereas cells overexpressing the wild type PS 2 cDNA produce robust levels of Abeta and p 3 . ^^^ These data suggest that PS 2 is functionally involved in Abeta production and Notch signaling by facilitating similar proteolytic cleavages . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The mutations occur in the genes encoding the beta amyloid precursor protein ( betaAPP ) and presenilin ( PS 1 ) and PS 2 and cause the increased secretion of the pathologically relevant 42 amino acid Abeta 42 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The genetics of familial AD ( FAD ) supports a central role for A beta in AD since mutations in the FAD causing genes APP and the presenilins ( PS 1 and PS 2 ) increase the formation of A beta 42 , 43 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| For example , age at onset and age at death between PS 1 , PS 2 , APP and sporadic AD groups differ . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| FAD associated mutations in PS 1 and PS 2 enhance the production of Abeta 42 , and PS 1 is required for physiological Abeta production , since a gene knockout of PS 1 and dominant negative mutations of PS 1 abolish Abeta generation . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The presenilin 1 ( PS 1 ) and PS 2 proteins are thought to play roles in processing of amyloid precursor protein ( APP ) , but the nature of this role is not fully understood . ^^^ We now show that PS 1 and PS 2 participate in other aspects of APP processing . ^^^ Transfection of PS 1 / cells with PS 2 is also able to correct the deficits in APP secretion , which suggests that the PS 2 also has the ability to regulate APP processing . ^^^ Finally , transfection of the truncated PS 2 construct , Alg 3 , into cells lacking PS 1 increases APP C terminal fragments . ^^^ This suggests that Alg 3 can interfere with the processing of APP by PS 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| These are the genes of the amyloid precursor protein ( APP ) and two presenilins ( PS 1 and PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Therefore , the co expression of PS 1 and PS 2 TM Asp > Ala mutants suppresses the formation of any detectable PS 1 or PS 2 heterodimeric fragments and essentially abolishes the production of Abeta . ^^^ Cells stably co expressing TM Asp > Ala mutations in both PS 1 and PS 2 show further accumulation of the APP derived gamma secretase substrates , C 83 and C 99 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Like the mutations identified within the betaAPP gene , mutations in PS 1 and PS 2 cause the increased generation of Abeta 42 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in genes encoding beta APP , presenilin ( PS ) 1 and PS 2 are known to cause FAD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We previously reported that mouse brains harboring mutant PS 2 contained increased levels of amyloid beta protein ( Abeta ) 42 in the Tris saline soluble fraction ( Oyama , F . , Sawamura , N . , Kobayashi , K . , Morishima Kawashima , M . , Kuramochi , T . , Ito , M . , Tomita , T . , Maruyama , K . , Saido , T . ^^^ The insoluble Abeta levels were found to be higher than the soluble Abeta levels , and the insoluble Abeta 42 levels were markedly increased in mutant PS 2 transgenic mice . ^^^ This fraction from two independent lines of mutant PS 2 transgenic mice contained remarkably increased levels of Abeta 42 and significantly low levels of glycerophospholipids and sphingomyelin . ^^^ This unexpected finding suggests that a large increase in the levels of Abeta 42 in mutant PS 2 mice is presumably induced through alterations of the lipid composition in the low density membrane domain in the brain . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| There is evidence that the polytopic membrane spanning proteins , presenilin 1 and 2 ( PS 1 and PS 2 ) , are important determinants of gamma secretase activity : mutations in PS 1 and PS 2 that are associated with early onset familial Alzheimer ' s disease increase the production of A beta 42 ( refs 4 6 ) , the more amyloidogenic peptide ; gamma secretase activity is reduced in neuronal cultures derived from PS 1 deficient mouse embryos ; and directed mutagenesis of two conserved aspartates in transmembrane segments of PS 1 inactivates the ability of gamma secretase to catalyse processing of APP within its transmembrane domain . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here we report that the APP C terminal fragments , C 83 and C 99 , which are the direct substrates of gamma secretase , can be coimmunoprecipitated with both PS 1 and PS 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Rare forms of autosomal dominant AD are caused by mutations in the APP and presenilin genes ( PS 1 and PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the genes encoding the presenilins ( PS 1 and PS 2 ) and amyloid precursor protein ( APP ) are associated with FAD , whereas mutations in the prion protein ( PrP ) gene are associated with prion disease . ^^^ In 12 patients , we found five novel mutations ( in PS 1 , F105L ; in PS 2 , T122P and M239I ; and in PrP , Q160X and T188K ) and five previously reported mutations ( in APP , in three patients who were most likely unrelated , V717I ; in PS 1 , A79V and M139V ; and in PrP , P102L and T183A ) that are all considered to be disease causing . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Heterozygous mutations in the genes for amyloid precursor protein ( APP ) , the presenilins ( PS 1 , PS 2 ) , prion protein ( PrP ) , neuroserpin , and tau are associated with early onset dementia ( EOD ) with or without neurological signs in the early disease stage . ^^^ In 12 patients , we found 5 novel mutations ( PS 1 : F105L ; PS 2 : T122P , M239I ; PrP : Q160X , T188K ) and 5 previously reported mutations ( APP : in three most likely unrelated patients V717I ; PS 1 : A79V , M139V ; PrP : P102L , T183A ) that all are considered disease causing . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Some of the genes are highly penetrant ( PS 1 , PS 2 , beta APP ) ; the other , APOE , is a weaker susceptibility factor . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin 2 ( PS 2 ; AD 4 ) , a regulator of intercellular signaling during CNS development and cell fate determination , appears to be involved in pathogenic processing of beta amyloid precursor protein ( betaAPP ) into potentially neurotoxic beta amyloid ( Abeta ) peptides . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In addition , calsenilin / DREAM / KChIP3 expression increased Ab 42 production in cells expressing APPsw , which was potentiated by PS 2 , but not by PS2 / 411stop , which suggests a role for apoptosis associated Ab 42 production of calsenilin / DREAM / KChIP3 . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Recently , PS 1 and PS 2 are shown to be the catalytic subunits of gamma secretase that cleave the intramembrane segments of beta APP and Notch . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin ( PS ) proteins facilitate endoproteolysis of selected type 1 transmembrane proteins such as the Alzheimer ' s disease ( AD ) associated beta Amyloid precursor protein ( beta APP ) and Notch . beta APP is cleaved within its transmembrane domain by an aspartyl protease activity termed gamma secretase , which may be identical with PS 1 and PS 2 . ^^^ ATF 6 processing also occurred in the presence of functionally inactive dominant negative mutants of PS 1 ( PS 1 D385N ) and PS 2 ( PS 2 D366A ) that do not support endoproteolysis of beta APP and Notch . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in three genes ( APP , PS 1 , and PS 2 ) cause familial Alzheimer ' s disease by alteration of the rate of generation of amyloid peptide or the length of this peptide . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Additionally , expression of mutant , but not wild type PS 2 , increased the production of beta amyloid protein ( Abeta ) 42 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We genotyped all family members for microsatellite markers at the IBGC 1 locus and polymorphisms of the ApoE , VLDL , alpha 1 ACT , BChE K , APP , PS 1 , PS 2 and tau genes and tested these for linkage to IBGC , dementia and bipolar disorder . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid plaques , primarily composed of Abeta , progressively develop in the brains of AD patients , and mutations in three genes ( APP , PS 1 , and PS 2 ) cause early onset familial AD ( FAD ) by directly increasing synthesis of the toxic , plaque promoting Abeta 42 peptide . ^^^ Recently , the gamma secretase has been tentatively identified as the presenilin proteins , PS 1 and PS 2 , and the identity of the beta secretase has been shown to be the novel transmembrane aspartic protease , beta site APP cleaving enzyme 1 ( BACE 1 ; also called Asp 2 and memapsin 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| RESULTS AND INTERPRETATION : We consider most of the proved etiological factors , especially the three genetic loci which have been shown to be associated with early onset AD : amyloid precursor protein ( APP ) gene , presenilin ( PS ) 1 and PS 2 genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| AD causing mutations in PS 1 and PS 2 result in a selective and significant increase in production of the more amyloidogenic Abeta 42 peptide . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilins ( PS 1 and PS 2 ) facilitate the final step in Abeta production , the intramembranous gamma secretase cleavage of amyloid precursor protein . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| BACKGROUND : Early onset familial Alzheimer ' s disease ( EOFAD ) is linked to mutations in three autosomal dominant genes : PS 1 , PS 2 and APP . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here we examined whether these presenilins are required for the generation of multiple A beta species by analyzing the production of several forms of secreted and intracellular A beta in mouse cells lacking PS 1 , PS 2 or both proteins . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| PS 1 and PS 2 are shown to be the catalytic subunits of gamma secretase that cleaves the intramembrane segments of beta APP and Notch . beta amyloid hypothesis that emphasizes the primacy of A beta in the pathogenesis of AD is currently being verified by the new experimental therapeutic approaches , e . g . , A beta vaccine therapy or administration of inhibitors of beta or gamma secretases . . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Main genes involved in AD include mutational loci ( APP , PS 1 , PS 2 , TAU ) and multiple susceptibility loci ( APOE , A2M , AACT , LRP 1 , IL1A , TNF , ACE , BACE , BCHE , CST 3 , MTHFR , GSK3B , NOS ) distributed across the human genome . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The multifactorial genetic dysfunction in AD includes mutational loci ( APP , PS 1 , PS 2 ) and diverse susceptibility loci ( APOE , A2M , AACT , LRP 1 , IL1A , TNF , ACE , BACE , BCHE , CST 3 , MTHFR , GSK3B , NOS 3 ) distributed across the human genome , probably converging in common pathogenic mechanisms that lead to premature neuronal death . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid plaques , primarily composed of Abeta , progressively develop in the brains of AD patients , and mutations in three genes ( APP , PS 1 , and PS 2 ) cause early on set familial AD ( FAD ) by increasing synthesis of the toxic Abeta 42 peptide . ^^^ Recently , the gamma secretase has been tentatively identified as the presenilin proteins , PS 1 and PS 2 , and the beta secretase has been shown to be the novel transmembrane aspartic protease , beta site APP Cleaving Enzyme 1 ( BACE 1 ; also called Asp 2 and memapsin 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| HN protects neuronal death caused not only by all known kinds of FAD genes ( mutant APP , PS 1 and PS 2 ) , but also by anti APP antibody and Abeta peptides , but not by long polyQ or SOD 1 mutants . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Recently , PS 1 and PS 2 are shown to be the catalytic subunits of gamma secretase that cleaves the intramembrane segments of beta APP and Notch . beta amyloid hypothesis that emphasizes the primacy of A beta in the pathogenesis of AD is currently being verified by the new experimental therapeutic approaches , e . g . , A beta vaccine therapy or administration of inhibitors of beta or gamma secretases . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| All the proteins ( APP , PS 1 , PS 2 ) encoded by AD related genes are involved in regulating neuronal apoptosis . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| AD appears to have a heterogeneous etiology with a large percentage termed sporadic AD arising from unknown causes and a smaller fraction of early onset familial AD ( FAD ) caused by mutations in one of several genes , such as the beta amyloid precursor protein ( APP ) and presenilins ( PS 1 , PS 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : Changes of learning and memory related gene expression , including mineralocorticoid receptor ( MR ) , presenile protein 1 and 2 ( PS 1 , PS 2 ) , tau , APP , apoE and bcl 2 in hippocampus of SAM were determined by reverse transcription polymerase chain reaction ( RT PCR ) . ^^^ RESULTS : Compared with those in the same aged mice , in the 5 month old SAM , levels of gene expression of MR , tau , PS 2 and APP were significantly higher , that of apo E lower , levels of gene expression PS 1 and bcl 2 were unobviously changed ; while in the 12 month old SAM , gene expression of MR and tau were higher , bcl 2 was lower and PS 1 , PS 2 , apoE and APP were also unobviously changed . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| It is notable that these differential effects parallel the differential effects of null mutations in PS 1 and PS 2 on APP and Notch processing . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations linked to AD such as those in presenilins 1 ( PS 1 ) and 2 ( PS 2 ) invariably increase the longer Abeta 42 species that forms neurotoxic oligomers . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Studies of the pathogenic mutations in presenilins 1 and 2 ( PS 1 and PS 2 ) and amyloid precursor protein ( APP ) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The discovery of pathogenic mutations in the amyloid precursor protein ( APP ) gene and the presenilin ( PS 1 , PS 2 ) genes , causing familial early onset AD has lead to the hypothesis of the amyloid cascade . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid plaques , composed primarily of Abeta progressively form in the brains of AD patients , and mutations in three genes ( amyloid precursor protein [ APP ] and presenilin 1 and 2 [ PS 1 and PS 2 ] ) cause early onset familial AD ( FAD ) by directly increasing production of the toxic , plaque promoting Abeta 42 peptide . ^^^ Several lines of evidence suggest that the PS 1 and PS 2 proteins are gamma secretase , and the identity of beta secretase has been shown to be the novel transmembrane aspartic protease , beta site APP cleaving enzyme 1 ( BACE 1 ; also called Asp 2 and memapsin 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilin ( PS 1 ) and ( PS 2 ) are the centers of gamma secretase that release Abeta from APP in Alzheimer ' s disease ( AD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| This review covers the trafficking and processing of APP , the amyloid cascade hypothesis in AD pathogenesis , the mutations in the genes encoding APP , PS 1 and PS 2 of early onset and late onset AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In addition , we measured the levels of proteins whose abnormal expression has been associated with neurodegeneration such as amyloid precursor protein ( APP ) , presenilin 1 and 2 ( PS 1 , PS 2 ) , and cyclooxygenases ( COX 1 and COX 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Structural genomics studies with AD related genes , including APP , MAPT , APOE , PS 1 , PS 2 , A2M , ACE , AGT , cFOS and PRNP genes , demonstrate different genetic profiles in AD and DVC , with an absolute genetic variation rate ranging from 30 to 80 % , depending upon genes and genetic clusters . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Transgenic animals have been created that express mutations in the amyloid precursor protein ( APP ) , presenilin ( PS ) 1 , and PS 2 , and also animals expressing more than one of these mutations . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Structural genomic studies with AD related genes , including APP , MAPT , APOE , PS 1 , PS 2 , A2M , ACE , AGT , cFOS , and PRNP , demonstrate different genetic profiles in AD and DVC , with an absolute genetic variation rate in the range of 30 80 % , depending upon genes and genetic clusters . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Twenty one unrelated patients with a history of suspected familial Alzheimer disease ( FAD ) were screened for mutations in PSEN 1 , PSEN 2 , and APP , the known FAD genes encoding the presenilins ( PS 1 and PS 2 ) and the amyloid precursor protein ( APP ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We report that the presenilins ( PS 1 and PS 2 ) also regulate Abeta degradation . ^^^ Neprilysin activity is restored by transient expression of PS 1 or PS 2 and by expression of the amyloid intracellular domain ( AICD ) , which is cogenerated with Abeta , during gamma secretase cleavage of betaAPP . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| This endoproteolytic activity cleaves within transmembrane domains of amyloid beta precursor protein ( APP ) and Notch , and familial Alzheimer ' s disease ( FAD ) mutations in PS 1 or PS 2 genes shift APP cleavage from production of amyloid beta ( Abeta ) 40 peptide to greater production of Abeta 42 . ^^^ Unlike PS 1 transgenes , wild type PS 2 transgenes expressed in the mouse CNS support little Abeta 40 or Abeta 42 production , and FAD PS 2 alleles support robust production of only Abeta 42 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Presenilins 1 and 2 ( PS 1 and PS 2 , respectively ) play a critical role in mediating gamma secretase cleavage of the amyloid precursor protein ( APP ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Macromolecular complexes containing presenilins ( PS 1 and PS 2 ) , nicastrin , anterior pharynx defective phenotype 1 ( APH 1 ) , and PS enhancer 2 ( PEN 2 ) mediate the intramembranous , gamma secretase cleavage of beta amyloid precursor protein ( APP ) , Notch , and a variety of type 1 membrane proteins . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The Abeta is derived from sequential cleavages of amyloid precursor protein ( APP ) by beta and gamma secretases . gamma Secretase consists of at least four proteins where presenilins ( PS 1 and PS 2 or PS ) are the catalytic subunit involved in the gamma site cleavage of APP . ^^^ Secretion of both Abeta 40 and Abeta 42 is significantly reduced in PS 1 knock out cells and completely abolished in cells deficient for both PS 1 and PS 2 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Interestingly PS 2 , a close homologue of PS 1 , appeared to be a less efficient producer of Abeta than PS 1 . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The multifactorial genetic dysfunction in dementia includes mutational loci ( APP , PS 1 , PS 2 , TAU ) and diverse susceptibility loci ( APOE , alpha2M , alphaACT , LRP 1 , IL 1 alpha , TNF , ACE , BACE , BCHE , CST 3 , MTHFR , GSK 3 beta , NOS 3 and many other genes ) distributed across the human genome , probably converging in a common pathogenic mechanism that leads to premature neuronal death , in which mitochondrial DNA mutations may contribute to increased genetic variability and heterogeneity . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Early onset familial Alzheimer ' s disease ( FAD ) is linked to autosomal dominant mutations in the amyloid precursor protein ( APP ) and presenilin 1 and 2 ( PS 1 and PS 2 ) genes . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the genes for amyloid precursor protein ( APP ) and presenilins ( PS 1 , PS 2 ) increase production of beta amyloid 42 ( Abeta 42 ) and cause familial Alzheimer ' s disease ( FAD ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| This is demonstrated by 1 ) genetic defects involving APP gene or APP dysfunction ( such as PS 1 or PS 2 ) , leading to the formation of neocortical amyloid plaques in familial AD ; 2 ) transgenic mice with these mutated genes that develop plaques ; 3 ) both sporadic and familial AD develop plaques . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Although the Ad 1 site ( TGACGTGA ) was similar to a palindromic CRE ( TGACGTCA ) , two other upstream sequences , Ad 3 and Ad 4 , were identified as the cAMP response sequences of the gene . ^^^ The effect of the mutation at the Ad 1 site on the cAMP response was almost the same as that of the deletion of Ad 3 and Ad 4 , although the role of each element seemed to be different . ^^^ These results indicated that both the Ad 1 site and the upstream elements , Ad 3 and Ad 4 , were necessary for the full response to cAMP of the CYP11B gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In endpoint titrations , fibroblast cultures showed an about 10 fold lower susceptibility towards Ad 1 and Ad 7 ; however , they compared favorably for Ad 4 , 8 , 12 , and 19 with HeLa or ( for Ad 8 ) with human amnion cell cultures . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| We have examined the transcriptional activity of four cis elements , Ad 1 ( CRE ) , Ad 2 , Ad 3 , and Ad 4 , that are present in the promoter of the bovine CYP11B ( 11 beta hydroxylase P 450 ) gene using beta globin reporter gene constructs and transient transfection into steroidogenic and nonsteroidogenic cell types . ^^^ The template carrying Ad 1 ( CRE ) and Ad 4 was also active in testicular Leydig cells , 1 10 , whereas it was inactive in nonsteroidogenic PC 12 cells . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| One epitope is unique to subgenus F adenoviruses ( Ad 40 and Ad 41 ) ; the other epitope is common to subgenus A ( Ad 12 , 18 and 31 ) and subgenus F ( Ad 40 , 41 ) adenoviruses but is not shared by representative serotypes of subgenera B ( Ad 3 and 7 ) , C ( Ad 1 , 2 and 5 ) , D ( Ad 8 ) or E ( Ad 4 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| This analysis shows that the release and aggregation of the A beta fragment from the amyloid precursor protein ( APP ) is involved in APP ( AD 1 ) , chromosome 14 ( AD 3 ) , 1 ( AD 4 ) and 19 ( AD 2 ) families as well as in the sporadic forms of AD , suggesting that AD is a single disease with a common APP / A beta amyloid pathogenesis . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In comparison with the CYP11B2 gene of other species , cis elements named Ad 1 , Ad 2 , Ad 3 , and Ad 4 , were identified in the 5 ' untranslated region of the hamster gene . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The antibodies used in the reagents consist of monoclonal antibodies against adenovirus type 3 ( Ad 3 ) , Ad 4 , Ad 8 , and adenoviruses of subgroup C ( Ad 1 , 2 , 5 , 6 ) , serotypes known to occur in outbreaks of disease . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here we show that in cultured HepG 2 cells wild type ( wt ) adenoviruses of subgroup A ( Ad 12 ) , B ( Ad 7 , 11 and 16 ) , C ( Ad 1 , 2 and 5 ) and E ( Ad 4 ) can efficiently mobilize Ad5CMVluc , a DeltaE1DeltaE3 Ad 5 vector carrying the firefly luciferase gene as reporter . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| RESULTS : On seven representative serotypes Ad 12 , Ad 3 , Ad 7 , Ad 11 , Ad 1 , Ad 8 , Ad 4 , the mean genome equivalents per ml and the mean 50 % infectious doses per ml were 10 ( 6 . 3 ) and 10 ( 4 ) , respectively . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : Using primers specific for the gene of ad 1 , ad 3 , ad 4 , ad 8 , ad 19 and ad 37 , heat denatured adenovirus DNA was amplified by the LAMP and polymerase chain reaction ( PCR ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| METHODS : Using primers specific for the gene of ad 1 , ad 3 , ad 4 , ad 8 , ad 19 and ad 37 , heat denatured adenovirus DNA was amplified by the LAMP and polymerase chain reaction ( PCR ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The slope of 1 . 06 in an allele , syt 1 ( AD 1 ) , which lacks the second Ca2+ binding domain , C2B , was not different from in syt 1 ( AD 4 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In this study , we evaluated the ability of low molecular weight thiol amides , N acetyl cysteine amide ( AD 4 ) that replenishes GSH levels , N acetyl glycine cysteine amide ( AD 7 ) and N acetyl Cys Gly Pro Cys amide ( CB 4 ) to protect primary neuronal culture against the oxidative and neurotoxic effects of Abeta ( 1 42 ) and to inhibit cisplatin and hydrogen peroxide induced phosphorylation of two MAP kinases ( MAPK ) , p 38 and ERK1 / 2 , in NIH3T3 cells . ^^^ Taken together , these results suggest that the thiol amides AD 4 , AD 7 and CB 4 protect neuronal cells against Abeta ( 1 42 ) toxicity by attenuating oxidative stress in correlation with inhibiting the MAPK phosphorylation cascade . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The activity and cellular localization of amylases was determined in 9 bacteria identified as Actinomyces israeli ( strains AA 2 and AD 4 ) , Bacteroides spp . ( strain AA 3 ) , Dichelobacter nodosus ( strain AA 4 ) , Mitsuokella multiacidus ( strain AA 6 ) , Eubacterium spp . ( strains AA 7 and AB 2 ) , Clostridium spp . ( strains AD 1 and AA 5 ) . ^^^ Four strains ( AA 3 , AA 4 , AA 5 , AD 4 ) produced extracellular amylases with an activity of 26 35 micromol of reducing sugars per h per mg of protein ; in five strains ( AA 2 , AA 6 , AA 7 , AB 2 , AD 1 ) amylases were membrane bound with an activity of 14 18 micromol of reducing sugars per h per mg of protein . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Over 100 rare , highly penetrant mutations have been described in three genes ( APP , PSEN 1 , PSEN 2 ) for early onset familial AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Recent estimates suggest that possibly over 70 % of the genetic variance for the disease remains unaccounted for by apolipoprotein E ( APOE ) and the three known early onset AD genes ( APP , PSEN 1 , PSEN 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| To date , mutations in three genes ( APP , PSEN 1 , PSEN 2 ) have been described to cause familial early onset AD . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in the amyloid precursor protein gene ( APP ) and the presenilin genes ( PSEN 1 en PSEN 2 ) cause early onset Alzheimer ' s disease . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| In cases of early onset Alzheimer ' s disease mutations of the presenilin genes ( PSEN 1 and PSEN 2 ) and APP can be found . ^^^ Mutations in the APP , PSEN 1 , and PSEN 2 genes were not identified . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Mutations in genes encoding amyloid precursor protein ( APP ) and presenilin 1 and 2 ( PSEN 1 , PSEN 2 ) are associated with increased accumulation of Abeta in neuritic plaques or in the walls of cerebral vessels . ^^^ All exons in genes encoding APP , PSEN 1 , PSEN 2 , cystatin C , transthyretin , gelsolin , and ITM2B were sequenced , and an association study of APP was conducted by identification of single nucleotide polymorphisms . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Fully penetrant ( causal ) mutations leading to predominantly early onset familial AD have been identified in three genes ( APP , PSEN 1 , PSEN 2 ) , while for the more common late onset form of the disease , only one partially penetrant genetic risk factor ( APOE ) has been established to date . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Cases of early onset AD have been attributed to three genes , PSEN 1 , PSEN 2 , and APP , while the only gene consistently associated with late onset AD ( LOAD ) is APOE . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Pathogenic mutations in the PSEN 1 and PSEN 2 genes encoding presenilin 1 and 2 , and the APP gene encoding amyloid b precursor protein , account for 18 50 % of familial EOAD cases with autosomal dominant pattern of inheritance . ^^^ A screening for mutations in the APP , PSEN 1 , and PSEN 2 genes is available to individuals with AD symptoms and at risk children or siblings of patients with early onset disease determined by a known mutation . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| For AD , three highly penetrant genes ( amyloid precursor protein ( APP , PSEN 1 and PSEN 2 ) and one susceptibility gene ( APOE ) have been identified . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Abeta , tau , and 7 of 8 other newly identified detergent insoluble proteins were disproportionately increased in temporal cortex from patients with LOAD and AD derived from mutations in PSEN 1 and PSEN 2 ; all of these except tau were elevated in individuals with prodromal dementia , while none except Abeta were elevated in aged APPswe mice . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Genetic studies of autosomal dominant early onset familial AD has identified three causative genes : amyloid precursor protein ( APP ) , presenilin 1 and 2 ( PSEN 1 and PSEN 2 ) . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| Despite the successes in the early 1990s when four genes were identified , which directly cause the disease ( APP , PSEN 1 and PSEN 2 ) or greatly increase the risk of disease development ( APOE ) , it has proved exceedingly difficult to identify additional genes involved in the pathogenesis . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| The varied ways in which mutations in presenilins ( PSEN 1 and PSEN 2 ) affect amyloid b precursor protein ( APP ) processing in causing early onset familial Alzheimer disease ( FAD ) are complex and not yet properly understood . ^^^ |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P49810 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|