◀ Back to IRS1
IRS1 — IRS2
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1-PIK3CA-PIK3R1)
(modification, collaborate)
Johnston et al., J Biol Chem 1995
Evidence: physical interaction
-
NCI Pathway Database IGF1 pathway:
IRS2/Crk complex (IRS2-CRK)
→
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
(modification, collaborate)
Beitner-Johnson et al., J Biol Chem 1996
Evidence: mutant phenotype, assay
-
NCI Pathway Database IL2-mediated signaling events:
IRS1-2 (IRS2/IRS1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1)
(modification, collaborate)
Johnston et al., J Biol Chem 1995
Evidence: physical interaction
-
Reactome Reaction:
IRS1
→
IRS2
(reaction)
Karas et al., Endocrinology 2001, Schreyer et al., Endocrinology 2003, Kim et al., Oncogene 2004, Rakatzi et al., Arch Physiol Biochem 2006, Bouzakri et al., Cell Metab 2006, Cuevas et al., J Hepatol 2007, Siemeister et al., J Biol Chem 1995, Xu et al., J Biol Chem 1995, Takahashi et al., Endocrinology 1997, Fantin et al., J Biol Chem 1998, Kim et al., Endocrinology 1998, Kim et al., J Biol Chem 1998
-
WikiPathways EPO Receptor Signaling:
Complex of GRB2-RAF1-SOS1-IRS2-JAK2-IRS1-RASA1
→
MAP2K1
(activation)
-
WikiPathways Insulin Signaling:
SHC3/IRS1/IRS2/SHC1/IRS4/SHC2/GAB1
→
Complex of IRS1-PIK3CA
(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
Kido et al., J Clin Invest 2000
(Diabetes Mellitus, Type 2...) :
These data indicate tissue-specific differences in the roles of IRSs to mediate insulin action, with
irs-1 playing a prominent
role in skeletal muscle and
irs-2 in liver
Richards et al., Endocrinology 2001
:
Collectively, these data suggest that the E2-induced decrease in uterine
insulin receptor substrate-2 requires IGF-I signaling, is not
dependent solely on
insulin receptor substrate-1 and PI3K, and is blocked by progesterone as well as by pharmacological inhibition of proteasomal protease activity
Valverde et al., Diabetes 2003
(Insulin Resistance) :
The lack of
IRS-2 did not
result in enhanced
IRS-1 tyrosine phosphorylation or IRS-1 associated phosphatidylinositol (PI) 3-kinase activity on insulin stimulation
Cui et al., Oncogene 2003
(Breast Neoplasms) :
We found that
insulin receptor substrate-2 (IRS-2) levels were markedly
induced by progesterone and the synthetic progestin R5020 in MCF-7 and other progesterone receptor (PR) positive breast cancer cell lines, whereas
IRS-1 and the IGF-I receptor were not induced
Zhou et al., Wei Sheng Yan Jiu 2006
(Insulin Resistance) :
IRS-1 ,
IRS-2 mRNA expression
increased in L and M ethanol groups but decreased in H ethanol group
Maeno et al., J Biol Chem 2012
(Metabolic Diseases) :
In this study, it was observed that PKC activation differentially
inhibited insulin receptor substrate 1/2 ( IRS1/2 ) signaling of insulin 's activation of PI3K/eNOS by decreasing only tyrosine phosphorylation of
IRS2
Bueno et al., Acta Cir Bras 2013
:
In contrast to the intestine,
IRS-1 ( p < 0.001 )
increased in the liver and
IRS-2 decreased ( p < 0.01 )
Rondinone et al., Proc Natl Acad Sci U S A 1997
(Diabetes Mellitus, Type 2) :
Gene disruption of
IRS-1 in mice is associated with an impaired insulin stimulated glucose disposal in vivo and glucose transport in vitro, but the survival of the animals and residual insulin sensitivity is
dependent on the presence of the alternative docking protein
IRS-2