| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| They were decorated with a PrP monoclonal antibody , but not with a beta A 4 antibody . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The F ( ab ' ) 2 of the patient ' s IgG had a synergetic effect on the aggregation of PRP induced by adenosine 5 diphosphate . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| RESULTS : APP had no negative effects on the quality of PRP . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The results lead to the conclusion that one cause of the AB effect is a locus at least as late as the PRP bottleneck . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In contrast , A beta 1 40 and prion peptide ( PrP ) 106 126 did not induce any significant increase in QUIN production . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In contrast , Abeta 11 40 and Prion peptide ( PrP ) 106 126 did not induce any significant increase in QUIN production . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Gene expression profiling in chronic copper overload reveals upregulation of Prnp and App . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Several cerebrovascular amyloid proteins ( amyloid beta protein ( Abeta ) , cystatin C ( ACys ) , prion protein ( AScr ) , transthyretin ( ATTR ) , gelsolin ( AGel ) , and ABri ( or A WD ) ) have been identified , leading to the classification of several types of CAA . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The colocalization patterns of both deposits were observed as being roughly of two types as follows : ( 1 ) diffuse beta protein deposits located around the PrP core ; and ( 2 ) a beta protein core and PrP core simultaneously existing in one amyloid plaque . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We used genomic DNA from 4 affected members of 2 families to determine whether the disease in these families is associated with a APP 717 mutation and the mutated codons , 102 , 117 , 129 , 178 and 200 , on the gene for protease resistance prion protein ( PrP ) which cause transmissible dementia , Creutzfelt Jacob disease ( CJD ) and Gerstmann Strausler syndrome ( GSS ) . ( ABSTRACT TRUNCATED AT 250 WORDS ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Multiple catalytic subunits of the Ca2+ and calmodulin ( CaM ) dependent protein phosphatase ( PrP ) ( `` calcineurin ' ' or PrP 2B ) are derived from at least two structural genes , type 1 ( `` calcineurin A alpha ' ' ) and type 2 ( `` calcineurin A beta `` ) , each of which can produce alternatively spliced transcripts . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Reducing oligosaccharides from the Haemophilus influenzae type b capsular polymer ( PRP ) coupled by reductive amination to diphtheria toxoids ( DTd ) had been shown to elicit potentially protective serum anti PRP antibodies ( Ab ) in infants too young for an adequate response to PRP vaccine . ^^^ Both vaccines consistently induced high anti PRP Ab responses in adults . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The addition of adenosine diphosphate ( ADP ) to platelet rich plasma ( PRP ) or to suspensions of washed platelets from the afibrinogenemic patients caused the formation of small aggregates , which was either not inhibited or only slightly inhibited by the F ( ab ' ) 2 fragments of an antibody to fibrinogen but was inhibited by an antibody ( 10E5 ) to glycoprotein IIb / IIIa . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Antisera were prepared against purified F ( ab ' ) 2 anti PRP from two unrelated adults , H . ^^^ T . anti PRP antibodies and F ( ab ' ) 2 fragments , and also reacted with the serum anti PRP antibodies from three additional adults unrelated to P . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Immunization of rabbits with the conjugates elicited antibody ( Ab ) to PRP and to DTx but not to a model for the linkage determinant . ^^^ Human adults given single subcutaneous injections had rises in serum Ab to PRP and in bactericidal activity in vitro ; the Ab protected infant rats challenged with Hib . ^^^ Rises in anti PRP Ab after the primary resembled the rises after PRP vaccine . ^^^ Development of bactericidal activity paralleled the rises in anti PRP Ab . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Well characterized antibodies against beta amyloid precursor protein ( beta APP ) and prion protein ( PrP ) , and specific cRNA probes , were used to localize beta APP and PrP and their mRNAs in human muscle macrophages . ^^^ Macrophages present in muscle biopsies of 51 patients with various neuromuscular disorders showed accumulation of beta APP and PrP , and strongly expressed beta APP and PrP mRNAs . ^^^ Our study provides the first demonstration that human muscle resident macrophages synthesize and accumulate beta APP and PrP . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We used genomic DNA from 8 sporadic cases to determine whether the disease in these families is associated with an APP 717 mutation and the mutated codons , 102 , 117 , 129 , 178 , and 200 , on the gene for proteinase resistant prion protein ( Prp ) which causes transmissible dementia , Creuzfelt Jacob disease ( CJD ) and Gerstmann Strussler syndrome ( GSS ) . ^^^ It would be necessary to analyze DNA from patient with sporadic Alzheimer ' s disease to examine the mutations found in the APP gene and Prp gene of heredity Alzheimer ' s disease patients . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| By light microscopy , PrP deposits co localized with beta amyloid protein ( A beta ) and ubiquitin ( Ub ) . ^^^ By immuno electronmicroscopy , both PrP and A beta were present on amorphous material and on 6 10 nm amyloid like fibrils ; and PrP and Ub co localized on cytoplasmic twisted tubulofilaments ( TTFs ) and on amorphous material . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| PrPc and APP serve as precursor proteins while modified PrP ( PrPsc and PrP 27 30 ) and beta A 4 as final deposits in transmissible and non transmissible brain amyloidoses , respectively . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The influence of acute , preoperatively performed plasmapheresis ( APP ) on platelet function was investigated in elective aortocoronary bypass patients subjected to APP producing either platelet poor plasma ( PPP ; group 1 ; n = 12 ) or platelet rich plasma ( PRP ; group 2 ; n = 12 ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Cytotoxicity of prion protein peptide ( PrP 106 126 ) differs in mechanism from the cytotoxic activity of the Alzheimer ' s disease amyloid peptide , A beta 25 35 . ^^^ We have used synchronous , clonal cell models originally developed to study the toxicity of the Alzheimer ' s disease amyloid peptide , A beta 25 35 , to investigate the actions of PrP peptides . ^^^ We found that the cytotoxicity of the PrP 106 126 depends on its state of aggregation and the cellular expression of PrPc , and is independent of a loss of MTT reduction activity in the absence of cell death associated with the cellular effects of A beta 25 35 . ^^^ The abnormal form of the prion protein ( PrPSc ) , a synthetic prion protein peptide fragment ( PrP 106 126 ) and fragments of the Alzheimer ' s protein precursor , APP , have been shown to be cytotoxic in vitro . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The immunolocalization of amyloid deposits containing either protease resistant prion protein ( PrP ) or amyloid beta protein ( A beta ) in the brains of patients with transmissible or non transmissible cerebral amyloidoses has been greatly facilitated by the pretreatment of tissue sections with concentrated formic acid . ^^^ Exposure of brain sections to microwaves , even for periods as brief as 1 sec , greatly enhanced the immunostaining of PrP and A beta amyloid deposits in both the transmissible and non transmissible brain amyloidoses . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| INTERVENTIONS : APP was performed between induction of anesthesia and incision , collecting either 10 mL / kg of autologous platelet poor plasma ( PPP patients , group 1 ; n = 20 ) or the same amount of platelet rich plasma ( PRP patients , group 2 ; n = 20 ) . ^^^ APP had no negative effects on the quality of PPP and PRP plasma . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Two anti ovine PrP peptide Ab raised in rabbits , 168 92 and 98 92 , confirmed that two separate cross reacting epitopes segregate with single aa differences between rabbit and sheep PrP at positions 43 and 99 of the rabbit PrP polypeptide . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The observation that PrP binds to a member of the APP ( amyloid precursor protein ) gene family is intriguing , in light of possible relevance to Alzheimer ' s disease . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In parallel with the determination of the effect of Flupirtine on the toxin ( A beta , PrP or glutamate ) induced neuronal death the effect of the drug on the intracellular Ca2+ level [ Ca2+ ] 1 , was measured . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| This review summarizes the main criteria for identification , and the presumed meaning of the chief markers indicating the presence of abnormally phosphorylated tau proteins , A beta peptides , and PrP proteins . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Examination of the N terminal sequence of non A beta component of Alzheimer ' s Disease amyloid ( NAC ) revealed a degree of similarity to regions crucial for aggregation and toxicity of three other amyloidogenic proteins , namely amyloid beta peptide ( A beta ) , prion protein ( PrP ) and islet amyloid polypeptide ( IAPP ) , leading us to believe that this might be the part of the molecule responsible for causing aggregation . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The prion protein ( PrP ) and the amyloid beta ( Abeta ) precursor protein ( APP ) are two normal proteins constitutively synthesised in human brain . ^^^ An altered form of PrP accumulates in Creutzfeldt Jakob disease , while Abeta is involved in the pathogenesis of Alzheimer ' s disease . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We are currently interested in a group of proteins associated with the dementias characterized by amyloid deposition in the brain : amyloid beta protein precursor ( A beta PP ) of Alzheimer ' s disease ( AD ) and the abnormal isoform of prion protein ( PrP ) of spongiform encephalopathies such as kuru , Creutzfeldt Jacob disease ( CJD ) and Gerstmann Straussler Scheinker disease ( GSSD ) . ^^^ Here we show that both A beta PP and prion protein ( PrP ) consist of peculiar internal repeats and share regions of sequence similarity . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| It is especially intriguing how the powerful catalytic redox activity of antioxidant Cu / Zn superoxide dismutase can convert into a pro oxidant activity , a theme echoed in the recent proposal that Abeta and PrP , the proteins respectively involved in Alzheimer ' s disease and prion diseases , possess similar redox activities . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the present study we have compared the interaction of apoE with A beta , the gelsolin derived amyloid fragment AGel ( 183 210 ) and the amyloidogenic prion fragments PrP ( 109 122 ) and PrP ( 109 141 ) . ^^^ We show that , similar to A beta , also AGel and PrP fragments can form a complex with apoE , and that the interaction between apoE and the amyloidogenic protein fragments is mediated through the same binding site on apoE . ^^^ |
|
| Interacting proteins: P04156 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 . ^^^ We found two mutations ( APP V717I ) in two of the three UFH patients , and only one mutation ( PrP T188K ) in 1 of the 17 patients with NFH . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Hence , this study compared the spatial patterns of prion protein ( PrP ) deposits in the cerebral cortex and hippocampus in cases of sporadic CJD with those of beta amyloid ( Abeta ) deposits in sporadic AD . ^^^ PrP and Abeta deposits were aggregated into clusters and , in 90 % of brain areas in CJD and 57 % in AD , the clusters were regularly distributed parallel to the tissue boundary . ^^^ In a significant proportion of cortical analyses , the mean diameter of the clusters of PrP and Abeta deposits were similar to those of the cells of origin of the cortico cortical pathways . ^^^ Abeta deposits in AD were distributed more frequently in larger sized clusters than PrP deposits in CJD . ^^^ In addition , in the hippocampus and dentate gyrus , clustering of Abeta deposits was observed in AD but PrP deposits were rare in these regions in CJD . ^^^ |
|
| Interacting proteins: P04156 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 . ^^^ We found 2 mutations ( APP V717I ) in 2 of the 3 the UFH patients , and only 1 mutation ( PrP T188K ) in 1 of the 17 patients with NFH . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Immunoprecipitation , electrophoresis and Western blot studies have shown that synaptophysin , amyloid precursor protein ( APP ) and betaA 4 do not co precipitate with PrP . ^^^ These results suggest that synaptophysin , APP and betaA 4 are likely not bound to PrP . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In all patients the PrP deposits were aggregated into clusters and , in 90 % of cortical areas and in 50 % of cerebellar sections , the clusters exhibited a regular periodicity parallel to the tissue boundary ; a spatial pattern also exhibited by beta amyloid ( Abeta ) deposits in Alzheimer ' s disease ( AD ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Both Creutzfeldt Jakob ( CJD ) and Alzheimer ' s disease ( AD ) are characterized by the deposition of insoluble beta pleated sheet peptides [ prion protein ( PrP ) and beta amyloid ( Abeta ) , respectively ] in the extracellular spaces of grey matter in the brain , but there is discordance in both diseases between the peptide levels in the brain and in the CSF . ^^^ In both diseases , facilitation of ISF drainage and elimination of PrP and Abeta peptides from the extracellular spaces of the brain may lead to practical therapeutic strategies for these devastating disorders . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid beta precursor protein ( APP ) and prion protein ( PrP ) are cell membrane elements implicated in neurodegenerative diseases . ^^^ It is proposed that PrP catalyses its own cleavage , the C terminal fragment functions as an alpha secretase and the N terminal segment chaperones the active site ; the alpha secretase releases anticoagulant and neurotrophic ectodomains from APP . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| This structural pattern revealed similarity to that observed previously in microglial cells producing fibrillar PrP amyloid in scrapie infected mice and Abeta in brains of human elderly patients and in Alzheimer ' s type brain pathology . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the temporal cortex , a few plaques were immunopositive for both PrP and Abeta ; the latter was expressed at the periphery of the PrP immunopositive cores . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| While different causes have usually been considered for PRP and AB phenomena , recent evidence has supported a unified account based on a single , shared restriction on concurrent processing . ^^^ Here we show that a full assessment of separate and shared resource limitations requires direct comparison of hybrid PRP / AB trials with corresponding pure PRP and AB cases . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the APP group , blood was withdrawn after induction of anesthesia , to sequester approximately 300 mL of platelet rich plasma ( PRP ) ; platelet poor plasma ( PPP ) and red blood cells ( RBC ) were sequestered as well . ^^^ After completion of the aortic reconstruction , autologous PRP and PPP were re infused in the APP group . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We report here that synthetic amyloid beta ( Abeta ) 1 42 and prion protein ( PrP ) 106 126 peptides promote macrophage survival ; they also induce macrophage DNA synthesis , particularly in the presence of sub optimal concentrations of the growth factor , macrophage colony stimulating factor ( M CSF or CSF 1 ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In Alzheimer ' s disease ( AD ) , amyloid deposition in the form of neuritic plaques and congophilic angiopathy is driven by the conversion of normal soluble amyloid beta ( sAbeta ) to Abeta plaques , whereas in the prionoses the critical event is the conversion of normal prion protein , PrP ( C ) , to PrP ( Sc ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| As Cu ( 2+ ) effects are reported in many other amyloidoses , e . g . , PrP , alpha synuclein , and Abeta , our results may be extended to the emerging field of divalent ion associated amyloidosis . . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In Alzheimer ' s disease , amyloid deposition in the form of neuritic plaques and congophilic angiopathy is driven by the conversion of normal soluble amyloid beta peptide ( sA beta ) to A beta plaques ; while in the prionoses the critical event is the conversion of normal prion protein , PrP ( C ) , to the disease associated form , PrP ( Sc ) . ^^^ Particularly interesting are compounds termed ' beta sheet breakers ' that directly target the abnormal conformational change both for A beta and PrP ( Sc ) related deposits . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| However , rarely described in GSS 102 , prominent p tau deposits as pretangles , neurofibrillary tangles and degenerating neurites were demonstrated adjacent to or around PrP plaques . beta Amyloid protein ( Abeta ) plaques were generally sparse and appeared invariably to be of a diffuse type . ^^^ Double labeling immunohistochemistry yielded co localization of p tau with PrP but not with Abeta . ^^^ Most PrP plaques did not contain Abeta . ^^^ Quantitative analysis on a fractional area density of immunoreactive pixels demonstrated that burdens of PrP and p tau but not Abeta were significantly correlated . ^^^ These results suggest that p tau deposition in this GSS 102 is secondarily induced by PrP but not by Abeta ( secondary tauopathy ) . ^^^ |
|
| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Using sequence alignments and structural analysis of the available nuclear magnetic resonance structures of PrP ( C ) , we explore the propensities of helices in PrP ( C ) to be in a beta strand conformation . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Alzheimer ' s disease ( AD ) and prion disease are characterized neuropathologically by extracellular deposits of Abeta and PrP amyloid fibrils , respectively . ^^^ The present data suggest that the cerebral Abeta and PrP deposits are closely associated with a locally induced , non immune mediated chronic inflammatory response . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| This cleavage occurs in an analogous way , in the middle of the ' toxic ' Abeta and PrP ( c ) 106 126 domains of betaAPP and PrP ( c ) , respectively . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The present article introduces the three amyloid diseases , AD , prion diseases and mouse senile amyloidosis in which Abeta , PrP ( Sc ) and AApoAII amyloid fibrils deposit respectively . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We observed that APP ( 135 156 ) , amyloid beta peptide ( A beta ( 1 40 ) ) , and PrP ( 59 91 ) all have copper reducing ability , with the APP ( 135 156 ) peptide being more potent than the other fragments . ^^^ Moreover , we identify His , Cys and Trp residues as key amino acids involved in the copper reduction of A beta , APP and PrP , respectively . ^^^ Two proteins related to neurodegenerative diseases have been described as copper binding proteins : the amyloid precursor protein ( APP ) , a protein related to Alzheimer ' s disease , and the Prion protein ( PrP ) , related to Creutzfeldt Jakob disease . ^^^ We used different synthetic peptides from APP and PrP sequences in order to evaluate the ability to reduce copper . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| To determine the specificity of this response for Abeta and whether it is related to cytotoxicity , we tested a diverse range of fibrillar peptides including amyloid beta ( Abeta ) , the fibrillar prion peptides PrP 106 126 and PrP 178 193 and human islet cell amylin . ^^^ Fibrillar PrP 106 126 and Abeta peptides bound recombinant APP and APLP 2 suggesting the accumulation of these proteins was mediated by direct binding to the fibrillated peptide . ^^^ We found that PrP 106 126 and the non toxic but fibril forming PrP 178 193 increased APP levels in cultures derived from both wild type and PrP ( c ) deficient mice indicating that fibrillar peptides up regulate APP through a non cytotoxic mechanism and irrespective of parental protein expression . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Transforming growth factor ( TGF ) beta 1 and platelet derived growth factor ( PDGF ) AB were higher in the Friadent Schtze PRP ( TGF beta 1 , 196 . 8 + / 109 . 6 ng / ml ; PDGF AB , 251 . 6 + / 115 . 4 ng / ml ) than in the Smart PRePTM ( TGF beta 1 , 77 . 2 + / 54 . 8 ng / ml ; PDGF AB , 208 + / 85 . 2 ng / ml ) . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| We studied whether codon 129 polymorphism of the PrP gene modulates the presence of tau and Abeta associated lesions among 188 patients over 70 years of age without evidence of dementia . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| It is proposed that the Cu2+ binding site of the A beta ( 1 42 ) formed channels is modulated with Cu2+ in a similar way to those of channels formed with the prion protein fragment PrP ( 106 126 ) , suggesting a possible common mechanism for Cu2+ modulation of A beta and PrP channel proteins linked to neurodegenerative diseases . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| A beta , PrP , and SP C harbour an alpha helix which is strongly predicted to form a beta strand , and in all cases investigated so far such alpha helix / beta sheet discordance correlates with the ability to form beta sheet aggregates and fibrils . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Here , we report that an anti DNA Ab , OCD 4 , as well as gene 5 protein , a well established DNA binding protein , capture PrP from brains affected by prion diseases in both humans and animals but not from unaffected controls . ^^^ Moreover , OCD 4 detects disease associated PrP > 10 times more efficiently than a widely used Ab to PrP . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| This result also raises questions regarding a current view of PrP ( Sc ) structure that transforms helix H 1 into a beta sheet conformation . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Unfolding consists of oligomeric ring like structure with the central cavity and has an ATP dependent protein Unfoldingg activity with broad specificity in vitro , of which targets included PrP in beta sheet form , alpha synuclein , and A beta protein . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Glucagon has the same amyloidogenic propensities as pathologically related peptides such as beta amyloid ( Abeta ) 1 42 and prion protein fragment ( PrP ) 106 126 including conformational change to a beta sheet rich structure and cytotoxic effects by activating caspases . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| To date 22 different polypeptides , including Abeta in Alzheimer ' s disease and PrP ( Sc ) in prion disorders , are known to re fold and assemble into highly organized fibrils , which associate with heparan sulfate ( HS ) proteoglycans to form tissue deposits called amyloid . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| However , both peptides took a random coil conformation in water , and over time the random coil transformed into a beta sheet structure with a significant percentage of helical conformation and beta turn structure in PrP ( 119 126 ) and PrP ( 121 127 ) , respectively , as observed with CD spectroscopy . ^^^ Monomeric PrP ( 119 126 ) was more toxic to astrocytes than the control Abeta peptide ; however , the fibrillar form of PrP ( 119 126 ) was less toxic to astrocytes . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Higher concentrations of transforming growth factor beta 1 ( TGF beta 1 ) and platelet derived growth factor AB ( PDGF AB ) were found in the PCCS PRP ( TGF / beta1 , 290 + / 95 ng / mL ; PDGF AB , 157 + / 62 ng / mL ) than in the Anitua PRGF kit PRP ( TGF beta 1 , 73 + / 26 ng / mL ; PDGF AB , 47 + / 21 ng / mL ) . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Despite PrPSc accumulation and prion propagation in the lymphoreticular system before detectable neuroinvasion , no Ab response to PrP has been detected , probably due to immune tolerance . ^^^ In addition , immunization with ralpha PrP led to production of predominantly IgG 1 isotype Ab in the sera , whereas after immunization with rbeta PrP , IgG2b was significantly produced . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Members of the ADAM ( a disintegrin and metalloproteinase ) family of zinc metalloproteases , notably ADAM 10 and TACE ( ADAM 17 ) display alpha secretase activity towards APP and appear to be responsible for the alpha cleavage of PrP ( C ) . ^^^ The amyloidogenic cleavage of APP by the beta and gamma secretases appears to occur preferentially in cholesterol rich lipid rafts , while the conversion of PrP ( C ) into the infectious form PrP ( Sc ) also appears to occur in these membrane domains . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Prion protein ( PrP ) has been localized to amyloid beta ( Abeta ) senile plaques in aging and Alzheimer disease , but it is unknown whether PrP is directly involved in plaque formation or represents a reaction to amyloid deposition . ^^^ To evaluate possible functional effects of PrP in Abeta plaque formation , we analyzed bigenic mice ( TgCRND8 / Tg7 ) , carrying mutant human amyloid precursor protein ( APP ) 695 ( APP ( Swed+Ind ) , TgCRND 8 ) as well as the wild type Syrian hamster prion protein gene ( sHaPrP , Tg 7 ) , showing Abeta plaques at 3 months of age as well as highly increased HaPrP ( c ) levels . ^^^ Double labelling immunofluorescence showed co localization of Abeta and PrP in virtually all plaques in the brains of both control and experimental animals . ^^^ Our data suggest that PrP promotes plaque formation , and that this hitherto unknown functional role of PrP appears to be mediated by increased Abeta aggregation rather than by altered APP transcription or processing . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Behavioral research has highlighted three major bottlenecks of information processing that can cripple our ability to consciously perceive , hold in mind , and act upon the visual world , illustrated by the attentional blink ( AB ) , visual short term memory ( VSTM ) , and psychological refractory period ( PRP ) phenomena , respectively . ^^^ A review of the neurobiological literature suggests that the capacity limit of VSTM storage is primarily localized to the posterior parietal and occipital cortex , whereas the AB and PRP are associated with partly overlapping fronto parietal networks . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Biological properties of Abeta and prion ( PrP ) peptides , including their potential to activate microglia , relate to Abeta and PrP peptide fibrillogenic abilities that are influenced by certain amyloid associated factors . ^^^ However , since small oligomers of amyloid forming peptides are more toxic to neurons than large fibrils , certain amyloid associated factors that enhance fibril formation , may sequester the potentially harmful Abeta and PrP peptides from the neuronal microenvironment . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| As both Abeta and PrP ( 106 126 ) trigger neurotoxicity and cell death , this ADAM dependent proteolytic attack could represent a valuable therapeutic target in order to deplete cells from these endogenous `` toxins ' ' and prevent the associated aggregates usually detected in affected brains . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The main proteins associated with Alzheimer ' s and prion diseases ( amyloid precursor protein ( APP ) and prion protein ( PrP ( C ) ) , respectively , have binding sites for copper and it has therefore been suggested that they play a role in copper metabolism . ^^^ Here , we review evidence indicating that the copper binding domains ( CuBD ) of APP and PrP ( C ) are able to modulate the oxidation state of copper , and prevent neurotoxic effects and memory impairments induced by copper . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Abs to the prion protein ( PrP ) can protect against experimental prion infections , but efficient Ab responses are difficult to generate because PrP is expressed on many tissues and induces a strong tolerance . ^^^ In this study , we compared Ab and T cell repertoires directed to PrP in wild type and PrP knockout ( Prnp o / o ) C57BL / 6 mice . ^^^ In Prnp o / o mice , Abs raised by PrP plasmid DNA immunization recognized only N terminal PrP peptides ; analyses of Ab responses after PrP peptide / CFA immunization allowed us to identify six distinct epitopes , five of which were also recognized by Abs raised by PrP peptides / CpG . ^^^ By contrast , in wild type mice , no Ab response was detected after PrP plasmid DNA or peptide / CFA immunization . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The finding may provide further insight into the elucidating of the molecular mechanism underlying the fibrillization of alpha Syn , Abeta and PrP as well as other amyloidogenic proteins . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| To examine the structure of the misfolded state , amyloid fibrils were grown from a beta form of recombinant mouse PrP ( residues 91 231 ) . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In addition , we also determined whether substances released by Abeta and PrP activated microglia induce neuronal death . ^^^ Cultures of rat brain microglia cells were treated with the synthetic peptides Abeta 1 40 , Abeta 1 42 and PrP 106 126 for different time periods . ^^^ Our results show that Abeta 1 40 and PrP 106 126 caused similar morphological changes in microglia and increased the production of nitric oxide and hydroperoxides . ^^^ An increase on inducible nitric oxide synthase expression was also observed in microglia treated with Abeta 1 40 or PrP 106 . ^^^ In cocultures of microglia neurons , it was observed that microglia treated with Abeta 1 40 or PrP 106 126 induced a comparable extent of neuronal death . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In this study , the effect of polyamidoamine ( PAMAM ) dendrimers ( generations 3rd , 4th , and 5th ) on amyloid aggregation of the prion peptide PrP 185 208 and the Alzheimer ' s peptide Abeta 1 28 was examined . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| A remarkable inhibition of MSA was obtained with propidium iodide , suggesting that AChE triggers PrP 106 126 and Abeta aggregation through a similar mechanism . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Key sequence and chemical similarities between prion protein ( PrP ) and Abeta indicate that similar therapeutic strategies might be applicable for the treatment of Alzheimer ' s and prion diseases . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Amyloid fibrils from prion peptide PrP 185 208 and Alzheimer ' s peptide Abeta 1 28 were produced in vitro , and their formation was monitored using the dye thioflavin T ( ThT ) . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In CJD and other prion diseases , the process is initiated by conformational changes of the cellular prion protein , or PrP ( C ) , into a beta sheet rich isoform , named PrP ( Sc ) , which acquires protease resistance and detergent insolubility . ^^^ Once generated , Abeta and PrP ( Sc ) are highly prone to misassembly under thermodynamically favourable oligomeric forms and protofibril / fibril structures . ^^^ The variety of physicochemical states exhibited by Abeta and PrP ( Sc ) is accounted for by distinct molecular forms with different amino and / or carboxyl termini and alternative conformations . ^^^ Unlike Abeta , PrP ( Sc ) is also infectious , and this feature poses public health concerns , as in the case of iatrogenic and variant CJD ( vCJD ) . ^^^ Several lines of evidence suggest that Abeta and PrP ( Sc ) are the main factors responsible for death of selected neuronal populations in brains of AD and prion disease ' s victims . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Prion ( PrP ) and amyloid beta ( Abeta ) peptides are involved in the neuronal loss that occurs in Prion disorders ( PrD ) and Alzheimer ' s disease ( AD ) , respectively , partially due to Ca ( 2+ ) dysregulation . ^^^ Here , we analyzed whether the ER mediated apoptotic pathway is involved in the toxic effect of synthetic PrP and Abeta peptides . ^^^ In PrP 106 126 and Abeta 1 40 treated cortical neurons , the release of Ca ( 2+ ) through ER ryanodine ( RyR ) and inositol 1 , 4 , 5 trisphosphate ( IP ( 3 ) R ) receptors induces ER stress and leads to increased cytosolic Ca ( 2+ ) and reactive oxygen species ( ROS ) levels and subsequently to apoptotic death involving mitochondrial cytochrome c release and caspases activation . ^^^ These results demonstrate that the early PrP and Abeta induced perturbation of ER Ca ( 2+ ) homeostasis is a death message that leads to neuronal loss , suggesting that the regulation of ER Ca ( 2+ ) levels may be a potential therapeutical target for PrD and AD . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Moreover , these compounds either did not inhibit or inhibited to a much lower extent the expression of the luciferase reporter regulated by a prion protein ( PrP ) mRNA 5 ' UTR , used as an alternative mRNA structure to counterscreen APP mRNA 5 ' UTR in stably transfected SH SY5Y cell lines . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| Decreased levels of beta amyloid peptide 1 42 ( Abeta 1 42 ) in cerebrospinal fluid ( CSF ) are a characteristic feature of Alzheimer ' s disease ( AD ) but recently were also observed in Creutzfeldt Jakob disease ( CJD ) . ^^^ We analyzed the CSF of patients with CJD , and AD and nondemented controls using a quantitative urea based Abeta sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot . ^^^ Like in AD and nondemented controls , we found a highly conserved pattern of carboxyterminally truncated Abeta 1 37 / 38 / 39 in addition to Abeta 1 40 / 42 also in CJD patients . ^^^ By the introduction of the ratio Abeta 1 39 to Abeta 1 42 , CJD and AD can effectively be differentiated . ^^^ We conclude that the immunoblot shows disease specific CSF Abeta peptide patterns in CJD and AD and suppose that measurement of the Abeta peptide pattern seems to be a promising diagnostic tool in the differential diagnosis of dementias . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| To clarify the relationship between amyloid formation and amyloid precursor protein ( APP ) , the brain sections from eight patients with Alzheimer ' s disease ( AD ) and four with Gerstmann Strussler Syndrome ( GSS ) were investigated immunohistochemically by the double immunostaining method . ^^^ The authors documented that anti APP labeled degenerative neurites surrounding kuru plaques in all four GSS patients . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| APP 717 , APP 693 , and PRIP gene mutations are rare in Alzheimer disease . ^^^ We also tested for the APP codon 693 mutation associated with hereditary cerebral hemorrhage with amyloidosis Dutch type , for PRIP gene missense mutations at codons 102 , 117 , and 200 , and for the PRIP insertion mutations which are associated with Creutzfeld Jakob disease and Gerstmann Straussler Scheinker syndrome . ^^^ Thus these APP and PRIP mutations are rare in both FAD and nonfamilial AD . . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In the trisomy 16 mouse , an animal model of DS , we found marked dysregulation of two developmentally regulated genes , App and Prn p . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The authors performed linkage analysis to APP , PS 1 , PS 2 , FTDP 17 , BRI , PI 12 , FND , HD like , SCA 4 , SCA 5 , SCA 10 , SCA 11 , SCA 13 , PARK 1 , PARK 2 , PARK 3 loci ; direct mutation analysis of HD , DRPLA , SCA 1 , SCA 2 , SCA 3 , SCA 6 , SCA 7 , SCA 8 , SCA 12 , and PRNP genes ; and sequencing of the PRNP open reading frame . ^^^ |
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| Interacting proteins: P04156 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 . ^^^ |
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| Interacting proteins: P04156 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 . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| PrPc and APP are amyloid precursors and PrPsc and beta A 4 are final deposits in transmissible and nontransmissible cerebral amyloidoses of Alzheimer ' s disease type , respectively . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| APP begets the Abeta peptide , whereas PrPC begets the malignant prion protein PrPSc . ^^^ However , these diseases have many common features impinging on the metabolism of neuronal membrane proteins : the amyloid precursor protein APP in the case of AD , and the cellular prion protein PrPC in PrD . ^^^ APP begets the Abeta peptide , whereas PrPC begets the malignant prion protein PrPSc . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The Kb values of PrPc Abs appear to be as strong as the anti BSA ( Ab to BSA ) and other reported Kb values for proteins of similar size to PrPc . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| In contrast , PrPC mobilization by Ab reduces the stimulatory properties of DC and the proliferative potential of responding T cells . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| The transition of prion protein from a mainly alpha structured isoform ( PrPC ) to a beta sheet containing protein ( PrPSc ) represents a major pathogenetic mechanism in prion diseases . ^^^ |
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| Interacting proteins: P04156 and P05067 |
Pubmed |
SVM Score :0.0 |
| MEK inhibitor PD 98059 and MMP 11 antibody ( Ab ) significantly inhibited in vitro invasive and in vivo metastatic abilities induced by PrPc . ^^^ |
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