Gene interactions and pathways from curated databases and text-mining

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MAPK14 — SHC1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Hunt et al., J Biol Chem 1999 : Role of interleukin (IL)-2 receptor beta-chain subdomains and Shc in p38 mitogen activated protein ( MAP ) kinase and p54 MAP kinase ( stress activated protein Kinase/c-Jun N-terminal kinase ) activation
Ursø et al., J Biol Chem 1999 : In contrast, the IGF-I receptor chimera mediated more effective Shc phosphorylation, association of Shc with Grb2, and activation of mitogen activated protein kinase compared with the insulin receptor chimera
Cousin et al., Biochem J 1999 : Glucose ( > 3 mM ) independently increased tyrosine-phosphorylation mediated recruitment of growth-factor bound protein 2 (Grb2)/murine sons of sevenless-1 protein ( mSOS ) and PI3'K to insulin receptor substrate (IRS)-1 and IRS-2, as well as SH2 containing protein (Shc) association with Grb2/mSOS and downstream activation of mitogen activated protein kinase and 70 kDa S6 kinase
Goetze et al., J Biol Chem 2000 : Insulin binding to the insulin receptor (IR) triggers its autophosphorylation, resulting in phosphorylation of Shc and the downstream activation of p42/p44 extracellular signal regulated kinase 1/2 mitogen activated protein kinase ( ERK1/2 ), which mediates insulin induced proliferation in vascular smooth muscle cells ( VSMC )
Song et al., Mol Endocrinol 2002 (Breast Neoplasms) : Overexpression of dominant negative Shc blocked the effect of E2 on MAPK , indicating a critical role of Shc in E2 action
Kornmann et al., Gastroenterology 2002 (Cell Transformation, Neoplastic...) : In vitro, TAKA-1 cells stably transfected with FGFR-1 IIIc exhibited increased basal growth ; enhanced basal tyrosine phosphorylation of FGFR substrate-2 (FRS2), Shc , and phospholipase Cgamma ; and increased activation of mitogen activated protein kinase ( MAPK )
Chen et al., J Biol Chem 2002 : Incubation of cells with the specific EGFR inhibitor AG4178 blocked MbetaCD induced phosphorylation of EGFR, SHC , phospholipase C-gamma, and Gab-1 as well as MAPK activation
Song et al., Proc Natl Acad Sci U S A 2004 : Down-regulation of Shc , ERalpha, or IGF-1R with specific small inhibitory RNAs all blocked E2-induced mitogen activated protein kinase phosphorylation
Crowe et al., BMC cancer 2004 (Carcinoma, Squamous Cell) : FAK recruitment of paxillin to the cell membrane correlates with Shc phosphorylation and activation of MAPK
Clemmons et al., Mol Endocrinol 2005 : Shc activation results in induction of MAPK
Lieskovska et al., J Biol Chem 2006 (MAP Kinase Signaling System) : Our previous studies have shown that IGF-I induced Shc phosphorylation is necessary for sustained activation of MAPK and increased cell proliferation of SMCs, and both Shc and the tyrosine phosphatase SHP-2 must be recruited to the membrane protein SHPS-1 in order for Shc to be phosphorylated
Myers et al., Mol Cell Biol 1994 : Coexpression of IRS-1 or IRS-1F-895 with the insulin receptor was required for insulin stimulated mitogenesis in 32-D cells, while expression of the insulin receptor alone was sufficient to mediate insulin stimulated tyrosine phosphorylation of Shc and activation of p21ras and mitogen activated protein ( MAP ) kinase
Gunn-Moore et al., Biochem J 1997 : Taken together, our data suggest that the apparent defect in MAPK activation caused by the kinase insert may result predominantly from an inhibition of high-affinity Shc binding, although a role for PLC gamma and PtdIns 3-kinase can not be completely excluded
Gotoh et al., Mol Cell Biol 1997 : Shc stimulates Ras/mitogen activated protein kinase ( MAPK ) through forming a complex with Grb2 at the phosphorylated tyrosine ( Y ) residue 317
Seno et al., Growth Factors 1998 : The refolded, modified rhCR-1 protein was found to be biologically active by its ability to inhibit beta-casein expression, to stimulate the tyrosine phosphorylation of Shc and the activation of MAPK and by its capacity to facilitate branching growth of mouse mammary epithelial cells in type I collagen gels
Maru et al., J Cell Physiol 1998 : Matrigel induced long lasting tyrosine phosphorylation of Shc , with recruitment of Grb-2 and microtubule associated protein kinase ( MAPK ) activation in both parental NP31 and NP31 transformed by ts-v-Ras, which was blocked by anti-beta1 integrin antibody
Lee et al., Pediatr Res 1998 : Shc 52 is an activator of Ras and mitogen activated protein kinase , whereas Shc 66 antagonizes Ras activation