Gene interactions and pathways from curated databases and text-mining

◀ Back to IL4

IL4 — IRS2

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Gingras et al., Mol Endocrinol 2000 (Breast Neoplasms) : IL-4 rapidly induced IRS-1 and IRS-2 phosphorylation in ZR-75-1 human breast cancer cell lines
Giallourakis et al., J Biol Chem 2000 : However, no differential activation of STAT6, Akt, IRS-2 , or p70 ( S6k ), in response to IL-4 , was observed in these cells
Zhu et al., J Exp Med 2000 : It was found that IL-4 induced phosphorylation of Janus kinases 1 and 3, IL-4R alpha, signal transducer and activator of transcription 6, and insulin receptor substrate 2 was strikingly but transiently inhibited by TCR ligation both in conventional and TCR transgenic T cells
Jiang et al., J Immunol 2001 : Fes mediates the IL-4 activation of insulin receptor substrate-2 and cellular proliferation ... Overexpression of kinase-inactive Fes blocks the IL-4 activation of insulin receptor substrate-2 , but not STAT6
Zamorano et al., Cell Res 2001 : IL-4 induced the tyrosine phosphorylation of IRS2 in resting B lymphocytes and in LPS- or CD40L activated blasts ... However, IL-4 induced association of IRS2 with GRB2 in B cell blasts
Gingras et al., J Steroid Biochem Mol Biol 2001 : We have also found that IL-4 rapidly induced IRS-1 and IRS-2 phosphorylation in these cell lines
Kelly-Welch et al., J Immunol 2004 : IL-4 induced tyrosine phosphorylation of IRS2 was elevated in Tg ( + ) B cells, whereas IL-4 induced phosphorylation of STAT6 was similar between Tg ( + ) and Tg ( - ) B cells
Prokopchuk et al., Br J Cancer 2005 (Pancreatic Neoplasms) : Interleukin-4 enhanced activity of MAPK, Akt-1, and Stat3 in IL-4-responsive, but not in IL-4-unresponsive MIA PaCa-2 cells ; however, IL-4 enhanced tyrosine phosphorylation of insulin receptor substrate-1 and -2 in all cell lines
O'Connor et al., J Immunol 2007 (Diabetes Mellitus, Type 2) : Examination of IL-4 signaling in db/db macrophages revealed that IL-4 dependent IRS-2/PI3K complex formation and IRS-2 tyrosine phosphorylation was reduced compared with db/+ macrophages ... These results indicate that in the db/db mouse model of T2D, macrophage expression of SOCS-3 is increased, and impaired IL-4 dependent IRS-2/PI3K formation induces a state of IL-4 resistance that disrupts IL-4 dependent production of IL-1RA
Heller et al., Science signaling 2008 : Type I IL-4Rs selectively activate IRS-2 to induce target gene expression in macrophages ... IL-4 induced highly efficient, gammaC dependent tyrosine phosphorylation of insulin receptor substrate 2 (IRS-2) , whereas IL-13 was less effective, even when phosphorylation of signal transducer and activator of transcription 6 ( STAT6 ) was maximal
Johnston et al., J Biol Chem 1995 : We report here that IL-2, IL-7, and IL-15, as well as IL-4 , rapidly stimulate the tyrosine phosphorylation of IRS-1 and IRS-2 in human peripheral blood T cells, NK cells, and in lymphoid cell lines
Izuhara et al., Biochem Biophys Res Commun 1996 : In both cell lines, IL-4 induced tyrosine phosphorylation of IRS-2 , association of PI3 kinase with IRS-2, and FES or a FES related protein
Takeda et al., J Mol Med (Berl) 1997 : Two cytoplasmic proteins, signal transducer and activator of transcription ( STAT ) 6 and IL4 induced phosphotyrosine substrate/insulin receptor substrate 2 ( 4PS/IRS2 ), are activated in IL4 signal transduction