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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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ADAM17 — MAPK3

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Zhan et al., J Cell Sci 2007 (Mechanotransduction, Cellular) : TACE release of TNF-alpha mediates mechanotransduction induced activation of p38 MAPK and myogenesis
Brill et al., Cardiovasc Res 2009 : TACE activation induced by hydrogen peroxide was dependent on p38 mitogen activated protein kinase signalling, whereas protein kinase C, phosphoinositide 3-kinase, and caspases were not involved
Yamashita et al., Journal of ovarian research 2009 : Activation of PKA, p38 MAPK and ERK1/2 by gonadotropins in cumulus cells is critical for induction of EGF-like factor and TACE/ADAM17 gene expression during in vitro maturation of porcine COCs ... The results showed that PKA, p38 MAPK and ERK1/2 positively controlled the expression of EGF-like factor and TACE/ADMA17 , the latter of which impacts the cumulus expansion and oocyte maturation of porcine COCs via the EGFR-ERK1/2 pathway in cumulus cells
Killock et al., Biochem J 2010 : The cytoplasmic domains of TNFalpha converting enzyme ( TACE/ADAM17 ) and L-selectin are regulated differently by p38 MAPK and PKC to promote ectodomain shedding
Liu et al., J Cell Biochem 2010 (Neuroblastoma) : Taken together, our data indicate that PLA(2) evoked p38 MAPK activation and ERK inactivation are involved in ADAM17 posttranscriptional up-regulation, and suggest that the action of PLA(2) is catalytic activity dependent
Liu et al., J Biol Chem 2010 : It was found that PILP-1 evoked p38 MAPK activation and ERK inactivation led to PILP-1 induced cell death and down-regulation of ADAM17
Van Schaeybroeck et al., Cancer Res 2011 (Colorectal Neoplasms) : Collectively, our findings indicate that oncogenic Kras regulates ADAM17 activity and thereby growth factor ligand shedding in a MEK1/2/Erk1/2 dependent manner and that KrasMT CRC tumors are vulnerable to MEK1/2 inhibitors, at least in part, due to their dependency on ADAM17 activity