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JAK2 — SH2B1

Pathways - manually collected, often from reviews:

• Reactome Reaction: JAK2 → SH2B1 (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, Nishi et al., Mol Cell Biol 2005, 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
• Reactome Reaction: JAK2 → SH2B1 (reaction) Nishi et al., Mol Cell Biol 2005, Li et al., Mol Endocrinol 2007, Gery et al., J Leukoc Biol 2009*
• Reactome Reaction: JAK2 → SH2B1 (direct_complex) Gery et al., J Leukoc Biol 2009*

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: JAK2 — SH2B1 (direct interaction, two hybrid) Nishi et al., Mol Cell Biol 2005
• IRef Biogrid Interaction: JAK2 — SH2B1 (physical association, affinity chromatography technology) Xie et al., Oncogene 2002*
• IRef Biogrid Interaction: JAK2 — SH2B1 (direct interaction, two hybrid) Rui et al., Mol Cell Biol 1997*
• IRef Biogrid Interaction: JAK2 — SH2B1 (direct interaction, pull down) Rui et al., Mol Cell Biol 1997*
• IRef Biogrid Interaction: JAK2 — SH2B1 (physical association, affinity chromatography technology) Rui et al., Mol Cell Biol 1997*
• IRef Biogrid Interaction: JAK2 — SH2B1 (physical association, affinity chromatography technology) Li et al., Mol Endocrinol 2007
• IRef Hprd Interaction: SH2B1 — JAK2 (in vivo) Rui et al., Mol Cell Biol 2000*, O'Brien et al., J Biol Chem 2003*, Rui et al., Mol Cell Biol 1997*
• IRef Hprd Interaction: SH2B1 — JAK2 (in vitro) Rui et al., Mol Cell Biol 2000*, O'Brien et al., J Biol Chem 2003*, Rui et al., Mol Cell Biol 1997*
• IRef Intact Interaction: SH2B1 — JAK2 (association, coimmunoprecipitation) Li et al., Mol Endocrinol 2007
• IRef Intact Interaction: SH2B1 — JAK2 (association, pull down) Nishi et al., Mol Cell Biol 2005

Text-mined interactions from Literome

Carter-Su et al., Recent Prog Horm Res 2000 : GH-induced binding of SH2-B to JAK2 via this site potently activates JAK2 , leading to enhanced tyrosyl phosphorylation of Stat proteins and other cellular proteins
Nishi et al., Mol Cell Biol 2005 : SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present
Li et al., Mol Endocrinol 2007 : In the absence of leptin, SH2B1 constitutively bound, via its non-SH2 domain region ( s ), to non-tyrosyl phosphorylated JAK2, and inhibited JAK2 ... In the absence of leptin, SH2B1 constitutively bound, via its non-SH2 domain region ( s ), to non-tyrosyl phosphorylated JAK2, and inhibited JAK2 ... Overexpression of SH2B1 enhanced both JAK2- and JAK2 ( Y813F ) -mediated tyrosine phosphorylation of IRS1 in response to leptin, even though SH2B1 did not enhance JAK2 ( Y813F ) activation ... These data suggest that constitutive SH2B1-JAK2 interaction, mediated by the non-SH2 domain region ( s ) of SH2B1 and the non-Tyr ( 813 ) region ( s ) in JAK2, increases the local concentration of SH2B1 close to JAK2 and inhibits JAK2 activity ... Leptin stimulated SH2B1-JAK2 interaction, mediated by the SH2 domain of SH2B1 and phospho-Tyr ( 813 ) in JAK2, promotes JAK2 activation, thus globally enhancing leptin signaling
Zhang et al., J Cell Biochem 2008 : Either peptide should disrupt the complex of a PSM dimer linked to IR via SH2 domains as proposed for PSM activation of tyrosine kinase JAK2
Duan et al., Zhong Nan Da Xue Xue Bao Yi Xue Ban 2010 (Obesity) : SH2B1 dramatically enhanced the leptin stimulated tyrosine phosphorylation of JAK2 and IRS2 in HEK293 cells stably expressing LRb ( HEK239 ( LRb ) )