Gene interactions and pathways from curated databases and text-mining

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IRS1 — JAK2

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

Liang et al., Endocrinology 1999 : Tyrosine phosphorylated JAK2 resulting from GH stimulation was included in the amino-terminal IRS-1 fusion precipitates ; however, neither tyrosine phosphorylation of JAK2 nor treatment of cells with GH before extraction was necessary for the specific JAK2-IRS-1 interaction to be detected
Li et al., Mol Endocrinol 2007 : JAK2 was required for leptin stimulated phosphorylation of insulin receptor substrate 1 (IRS1) , an upstream activator of the phosphatidylinositol 3-kinase pathway
Girasol et al., PloS one 2009 : Surprisingly, some of these effects are dependent on signal transduction through the IRS1/PI3-kinase , but not on the activation of JAK2
Britschgi et al., Cancer Cell 2012 (Breast Neoplasms...) : Mechanistically, PI3K/mTOR inhibition increased IRS1 dependent activation of JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors
Burfoot et al., J Biol Chem 1997 : Janus kinase dependent activation of insulin receptor substrate 1 in response to interleukin-4, oncostatin M, and the interferons ... For the mutant human fibrosarcoma cell lines, phosphorylation of IRS-1 through the insulin-like growth factor receptor is independent of JAK1, JAK2 , or Tyk2
Thirone et al., Endocrinology 1999 : The correlation between JAK2 tyrosyl phosphorylation and IRS-1 tyrosyl phosphorylation in response to GH together with the results of the in vitro tyrosine kinase assay are consistent with the hypothesis that JAK2 may mediate GH-induced phosphorylation of IRS-1