Gene interactions and pathways from curated databases and text-mining

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IGF2 — IRS2

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Rui et al., J Biol Chem 2001 (Carcinoma, Hepatocellular...) : In this study, we show that insulin, IGF-1 , or osmotic stress promoted ubiquitin/proteasome mediated degradation of IRS-2 in 3T3-L1 cells, Fao hepatoma, cells and mouse embryo fibroblasts ; however, insulin/IGF-1 did not promote degradation of IRS-1 in 3T3-L1 preadipocytes or mouse embryo fibroblasts
Vincent et al., Neurobiol Dis 2004 : IGF-I : IGF-IR signaling involves phosphorylation of IRS-1 and Shc, but not IRS-2
Boissan et al., Am J Pathol 2005 (Carcinoma, Hepatocellular...) : The functionality of IRS-2 was demonstrated in Hep 3 B cells, in which IRS-2 tyrosine phosphorylation and its association with phosphatidylinositol-3 kinase were induced by IGF-2
Kim et al., Endocrinology 2005 (Neuroblastoma) : In summary, 1 ) IRS-2 is more sensitive to IGF-I mediated degradation ; 2 ) IRS degradation is mediated by phosphatidylinositol 3-kinase and proteasome sensitive pathways ; and 3 ) high levels of IGF-IR , and possibly the subsequent increase in Akt phosphorylation, are required for efficient IRS degradation
Barnes et al., Clin Cancer Res 2007 (Head and Neck Neoplasms) : Pretreatment of serum starved 183A or TU159 SCCHN cell lines with A12 ( 10 microg/mL ) blocked IGF stimulated activation of IGF-IR, insulin receptor substrate (IRS)-1 and IRS-2 , mitogen activated protein kinase, and phosphatidylinositol 3-kinase
Heckman et al., Dev Biol 2007 : Because both IGF and p190-B signaling affect IRS-1/2 , we examined IRS-1/2 double knockout embryonic mammary buds
Simmons et al., Am J Physiol Gastrointest Liver Physiol 2007 : In contrast, IGF-I activated both IRS-1 and IRS-2 in intestinal myofibroblasts and IRS-2 activation was upregulated in IRS-1-null myofibroblasts
Kwon et al., Cancer Res 2009 (Adenocarcinoma...) : Furthermore, we also showed that insulin receptor substrate (IRS)-2 , but not IRS-1, is involved in regulation of IGF-IR expression, which is most likely not transcriptional control ... Overall, these findings suggest a novel regulatory role of IRS-2 on the expression of IGF-IR through PKCdelta and mTOR in pancreatic cancer cells
Fukushima et al., J Biol Chem 2012 : In these cells, IGF-I stimulation induced tyrosine phosphorylation of IGF-IR and IRS-1/2 , but mutated IGF-IR failed to bind PI3K and to induce maximal phosphorylation of GSK3ß and cell proliferation in response to IGF-I
Dews et al., Recept Signal Transduct 1997 : Although the mitogenic function of the IGF-IR may require the activation of insulin receptor substrate-1 (IRS-1) or IRS-2 , an overexpressed IGF-IR is able to protect 32D cells, which lack IRS-1 and IRS-2, from apoptosis caused by Interleukin-3 (IL-3) withdrawal
Kornmann et al., Cancer Res 1998 (Colonic Neoplasms...) : Insulin, IGF-I , and IGF-II enhanced the growth of both cell lines, stimulated tyrosine phosphorylation of IRS-2 , and increased IRS-2 associated phosphatidylinositol (PI) 3-kinase activity
Kim et al., J Biol Chem 1998 (Neuroblastoma) : In contrast, IGF-I induces a transient tyrosine phosphorylation of IRS-2 and an association of IRS-2 with Grb2