◀ Back to IRS1
IRS1 — JAK2
Pathways - manually collected, often from reviews:
-
BioCarta growth hormone signaling pathway:
GH/GH R/GH R/JAK2/JAK2 complex (GHR-JAK2-GH1)
→
IRS-1 (IRS1)
(modification, activates)
-
Reactome Reaction:
IRS1
→
JAK2
(reaction)
Duan et al., J Biol Chem 2004, Li et al., Mol Endocrinol 2007
-
Reactome Reaction:
IRS1
→
JAK2
(indirect_complex)
Szanto et al., Proc Natl Acad Sci U S A 2000, Martín-Romero et al., Cell Immunol 2001, Duan et al., J Biol Chem 2004, Li et al., Mol Endocrinol 2007, Hill et al., J Clin Invest 2008, Buettner et al., Nat Med 2008, Bjørbaek et al., J Biol Chem 1997
-
WikiPathways EPO Receptor Signaling:
Complex of GRB2-RAF1-SOS1-IRS2-JAK2-IRS1-RASA1
→
MAP2K1
(activation)
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