Pubmed abstracts for Protein-Protein Interaction search result :


Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.5132541
SOCS 5 associated with the EGF R complex in an EGF independent manner , and the mitogenic response to EGF of all SOCS 5 expressing cell lines was dramatically inhibited when compared with control cell lines . 0.5132541^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
SOCS36E , a novel Drosophila SOCS protein , suppresses JAK / STAT and EGF R signalling in the imaginal wing disc . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
It is conceivable that combinatorial receptor interactions diversify signal transduction and confer double regulation , in cis and in trans , of the superior mitogenic activity of the kinase defective ErbB 3 . . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
HTF can also bind , but with a lower affinity , to a related cis sequence present in the epidermal growth factor receptor promoter . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
VEGF , bFGF , IL 8 , and MMP 9 expression was increased in muscle invasive compared with superficial papillary tumors , ( p < 0 . 05 ) and VEGF expression was increased in muscle invasive tumors compared with CIS specimens ( p < 0 . 05 ) . bFGF , IL 8 , and EGFR expression was increased in CIS specimens compared with superficial papillary tumors ( p < 0 . 05 ) . ^^^ The pattern of expression of bFGF , VEGF , IL 8 , MMP 9 , and EGFR represent the divergent developmental pathways in the pathogenesis of bladder TCC , which characterizes superficial or invasive bladder cancer . bFGF , IL 8 , and EGFR appear to be upregulated in early precursor lesions ( CIS ) , whereas VEGF appears to be upregulated at later stages in the development of muscle invasive TCC . . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
In the present study , the levels of EGFR were determined in serum from 38 patients with cervical carcinoma [ invasive or recurrent carcinoma ( n = 26 ) and carcinoma in situ ( CIS ; n = 12 ) ] and 38 healthy female controls using ELISA . ^^^ The mean serum level for EGFR in patients with invasive or recurrent carcinoma ( 165 + / 60 fmol / ml ) was significantly elevated ( P < 0 . 0001 ) compared with that of healthy controls ( 66 + / 17 fmol / ml ) and also higher ( P = 0 . 015 ) than that of patients with CIS ( 126 + / 25 fmol / ml ) . ^^^ In addition , there was a significant difference in the mean serum levels of EGFR between patients with CIS and healthy controls ( P < 0 . 0001 ) . ^^^ Thirty five patients ( 92 % ) with cervical carcinoma [ invasive or recurrent ( n = 24 ) and CIS ( n = 11 ) ] had elevated serum , EGFR levels above the cutoff value of 100 fmol / ml ( defined as 2 SD above the mean of the controls ) . ^^^ In conclusion , the serum EGFR level was elevated in a significant proportion of patients with cervical carcinoma , and it demonstrated an increasing tendency according to disease progression from normal tissue through CIS to invasive cervical carcinoma . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Amplification of the EGFR gene was observed in three cases ( 17 % ) of ED , one case of CIS and four cases ( 20 % ) of SCC . ^^^ In cases showing EGFR gene amplification , the degree of amplification was low in ED and CIS cases , whereas it was extremely high in SCC cases . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
A global EGF R score of > 5 was reached only in one metaplasia , in six SD , in six CIS and in six microinvasive tumours . ^^^ There was no difference in EGF R expression between normal , hyperplastic and metaplastic epithelia versus mild dysplasia or between severe dysplasia versus CIS and microinvasive tumours but there was a statistically significant difference between mild versus severe dysplasia . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
The EGFR expression rate increases from normal epithelium to carcinoma in situ ( CIS ) with a significant difference between mild versus severe dysplasia . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Four of six tumors analyzed showed a secondary somatic activating EGFR mutation , arising in cis with the germline EGFR mutation T790M . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Elevated levels of FGFR 3 , EGFR2 / neu , p 53 and to a lesser extent EGFR 1 and Raf 1 expression in the urothelial dysplasia and CIS were evident for patients of group 1 . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Addition of the epidermal growth factor receptor ( EGFR ) inhibitors PP 3 or AG 490 or the Src kinase inhibitor PP 2 blocked the SOCS 2 induced neurite outgrowth . ^^^ The overexpressed SOCS 2 bound to the EGFR , which was constitutively phosphorylated at Tyr 845 , the Src binding site . ^^^ Our findings suggest that SOCS 2 regulates EGFR phosphorylation , leading to regulation of neurite outgrowth through a novel pathway that is distinct from GH . . ^^^ SOCS 2 induces neurite outgrowth by regulation of epidermal growth factor receptor activation . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Tkip also inhibited epidermal growth factor receptor autophosphorylation , consistent with the fact that epidermal growth factor receptor is regulated by SOCS 1 and SOCS 3 , similar to JAK 2 . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Two Drosophila suppressors of cytokine signaling ( SOCS ) differentially regulate JAK and EGFR pathway activities . ^^^ Nonetheless , both SOCS regulate JAK and EGFR signaling pathways , albeit differently . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Notably , SOCS36E , the Drosophila ortholog of mammalian SOCS 5 , was recently implicated as a negative regulator of the Drosophila ortholog of EGFR . ^^^ In this study , we aimed at characterizing the role of SOCS 5 in the negative regulation of EGFR . ^^^ Here we show that the expression of SOCS 5 and its closest homolog SOCS 4 is elevated in cells following treatment with EGF , similar to several negative feedback regulators of EGFR whose expression is up regulated upon receptor activation . ^^^ The expression of SOCS 5 led to a marked reduction in EGFR expression levels by promoting EGFR degradation . ^^^ The reduction in EGFR levels and EGF induced signaling in SOCS 5 expressing cells requires both the Src homology 2 and SOCS box domains of SOCS 5 . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
In addition , we found that receptor tyrosine kinases such as platelet derived growth factor receptor or epidermal growth factor receptor can very potently phosphorylate IL 6 induced SOCS 3 . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Evaluation of epidermal growth factor receptor ( EGFR ) by chromogenic in situ hybridization ( CISH ) and immunohistochemistry ( IHC ) in archival gliomas using bright field microscopy . ^^^ EGFR gene amplification and chromosome 7 aneuploidy was detected in 34 formalin fixed , paraffin embedded benign and malignant gliomas by chromogenic in situ hybridization ( CISH ) using digoxigenin labeled EGFR and biotin labeled chromosome 7 centromeric probes . ^^^ Simultaneous detection of EGFR gene copies or chromosome 7 centromere signals along with tissue morphology allows us to compare CISH results easily with IHC results . ^^^ Our results show that CISH is an objective , practical , and accurate assay to screen for EGFR gene status in gliomas . . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
We studied EGFR gene amplification by chromogenic in situ hybridization ( CISH ) and protein expression by immunohistochemistry in 175 breast carcinomas , using tissue microarrays . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Gene amplification of EGFR was examined by two in situ hybridization techniques , fluorescence in situ hybridization ( FISH ) and chromogenic in situ hybridization ( CISH ) in serial sections to IHC . ^^^ Only 1 of 14 EGFR positive breast cancers showed gene amplification at low levels by CISH . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
We have therefore used CISH as an efficient , economic and reliable means for routinely assessing EGFR amplification in GBM , including the small cell variant . . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
METHODS : EGFR and HER 2 gene amplification was examined in atypical adenomatous hyperplasia ( AAH ) , bronchioloalveolar carcinoma ( BAC ) , and adenocarcinoma with mixed subtypes ( MX ) by chromogenic in situ hybridisation ( CISH ) , and protein expression was examined by immunohistochemistry using paraffin wax embedded tissues . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
Chromogenic in situ hybridization ( CISH ) was used to detect amplification of the epidermal growth factor receptor ( EGFR ) gene in tissue microarrays of tumours derived from 287 patients with grade 2 4 diffuse astrocytomas . ^^^ Our data verify the central role of EGFR in the pathobiology of astrocytic tumours , and highlight the advantages of CISH as a simple and practical assay to screen for EGFR gene amplification in astrocytic tumours . . ^^^
Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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Interacting proteins: Q9NSE2 and P00533 Pubmed SVM Score :0.0
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