Gene interactions and pathways from curated databases and text-mining

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IRS2 — PIK3R1

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

Shaw et al., Mol Cell Biol 2001 (Neoplasm Invasiveness) : Moreover, we identified a tyrosine residue in the cytoplasmic domain of the beta4 subunit, Y1494, that is required for alpha6beta4 dependent phosphorylation of IRS-2 and activation of PI3K in response to receptor ligation
Richards et al., Endocrinology 2001 : Collectively, these data suggest that the E2-induced decrease in uterine insulin receptor substrate-2 requires IGF-I signaling, is not dependent solely on insulin receptor substrate-1 and PI3K , and is blocked by progesterone as well as by pharmacological inhibition of proteasomal protease activity
Standaert et al., Endocrinology 2002 : Presently, in 3T3/L1 adipocytes, rosiglitazone induced sizable increases in basal glucose transport that were : dependent on PI3K, 3-phosphoinositide dependent protein kinase-1 ( PDK-1 ), and PKC-lambda ; accompanied by increases in tyrosine phosphorylation of Cbl and Cbl dependent increases in PI3K and PKC-lambda activity ; but not accompanied by increases in IRS-1/2 dependent PI3K or protein kinase B activity ... Additionally, rosiglitazone increased IRS-1 and IRS-2 levels, thereby enhancing insulin effects on IRS-1- and IRS-2 dependent PI3K and downstream signaling factors PKC-lambda and protein kinase B
Pirola et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Conversely, adenoviral-driven expression of constitutively active PI3K induced an insulin independent reduction in IRS-1/2 protein levels
Miura et al., Biochemistry 2004 : Although insulin receptor substrate-1 (IRS-1) and IRS-2 , among other factors, activate PI3K , there is little information on the relative roles of IRS-1and IRS-2 during aPKC activation by insulin action in specific cell types ... These findings provide evidence that directly links both IRS-1 and IRS-2 to aPKC activation in immortalized brown adipocytes, and further suggest that IRS-1 and IRS-2 are required for the activation of Cbl/PI3K during insulin action in these cells
Gelling et al., Cell Metab 2006 (Diabetes Mellitus, Experimental) : Conversely, increased PI3K signaling induced by hypothalamic overexpression of either IRS-2 or protein kinase B ( PKB, a key downstream mediator of PI3K action ) enhanced the glycemic response to insulin by approximately 2-fold in STZ-DM rats
O'Connor et al., J Immunol 2007 (Diabetes Mellitus, Type 2) : In this study, we report that normal IL-4 dependent elaboration of IL-1 receptor antagonist (IL-1RA) requires IRS-2 mediated PI3K activity in primary macrophages
Szabolcs et al., Am J Pathol 2009 (Disease Progression...) : Because activation of PI3K signaling leads to feedback inhibition of insulin receptor substrate-2 (IRS2) expression, an upstream activator of PI3K, we therefore anticipated that IRS2 expression would be low in tumors that lack PTEN
Aoki et al., Am J Physiol Endocrinol Metab 2009 : In the livers of p85alpha-deficient mice, p50alpha played a compensatory role in insulin stimulated PI3K activation by binding to insulin receptor substrate (IRS)-1/2
Udelhoven et al., J Endocrinol 2010 : Thus, alternative binding of ZBP89 or SP1 to the described region in the IRS2 promoter regulates neuronal IRS2 expression in a PI3K dependent manner
Kim et al., Endocrinology 1998 (Neuroblastoma) : We also observed a concomitant increase in the mobility of IRS-2, suggesting that PI 3-K mediates or is required for IRS-2 serine/threonine phosphorylation, and that this phosphorylation inhibits IRS-2 tyrosine phosphorylation