Pubmed abstracts for Protein-Protein Interaction search result :


Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
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Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
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Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
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Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
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Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
Here we show that the GPCR kinase interacting protein 1 ( GIT 1 ) is a substrate for c Src that undergoes tyrosine phosphorylation in response to angiotensin 2 ( AngII ) and EGF in vascular smooth muscle and 293 cells . ^^^ We propose that GIT 1 is a novel regulator of PLCgamma function that mediates PLCgamma activation by c Src and integrates signal transduction by GPCRs and TKRs . . ^^^ GIT 1 mediates Src dependent activation of phospholipase Cgamma by angiotensin 2 and epidermal growth factor . ^^^ GIT 1 associates with PLCgamma via the PLCgamma Src homology 2 and 3 domains constitutively , and the interaction is unaltered by AngII and EGF . ^^^
Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
Here we show that the GPCR kinase interacting protein 1 ( GIT 1 ) is a substrate for c Src that associates with MEK 1 in vascular smooth muscle cells and human embryonic kidney 293 cells . ^^^ We propose that GIT 1 serves as a scaffold protein to facilitate c Src dependent activation of MEK 1 ERK1 / 2 in response to both GPCRs and TKRs . . ^^^
Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
Because Src is required for both GIT 1 tyrosine phosphorylation and focal adhesion disassembly , we studied the effects of Src on GIT 1 ERK1 / 2 interactions . ^^^
Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
The absence of either FAK or Src family kinases prevents PKL phosphorylation and suppresses localization of PKL but not GIT 1 to focal adhesions after Rac activation . ^^^
Interacting proteins: Q9Y2X7 and P12931 Pubmed SVM Score :0.0
Cell signaling molecules c src , G protein coupled receptor kinase interacting protein ( GIT 1 ) , and c jun N terminal kinase ( JNK ) were up regulated in endothelial cells from the same areas , whereas an increase in expression of junctional adhesion molecule 1 ( JAM 1 ) in blood vessels and infiltrating macrophages from inflammatory regions might form part of a leukocyte rolling response , increasing the plaque volume . ^^^