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IRS1 — RPS6KB1
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
Shah et al., Mol Cell Biol 2006
(Tuberous Sclerosis) :
Using two cell culture models of the familial hamartoma syndrome, tuberous sclerosis, we show here that Raptor-mTOR and
S6K1 are
required for phosphorylation of
IRS1 at a subset of serine residues frequently associated with insulin resistance, including S307, S312, S527, S616, and S636 ( of human IRS1 )
Bae et al., Hepatology 2007
(Hypoglycemia...) :
Oltipraz treatment inhibited the ability of TNF-alpha to activate p70 ribosomal
S6 kinase-1 ( S6K1 ) downstream of mammalian target of rapamycin, thus
preventing insulin receptor substrate-1 serine phosphorylation and protecting insulin signals
Tremblay et al., Proc Natl Acad Sci U S A 2007
(Insulin Resistance...) :
However, the
role of
S6K1 in mediating
IRS-1 phosphorylation in a physiological setting of nutrient overload is unresolved
Martin et al., J Biol Chem 2007
(Hyperplasia) :
Here, we show that rapamycin activates Akt and induces contractile protein expression in human VSMC in an insulin-like growth factor I-dependent manner, by relieving
S6K1 dependent negative regulation of
insulin receptor substrate-1 (IRS-1) ... In skeletal muscle and adipocytes, rapamycin relieves
mTOR/S6K1 dependent inhibitory phosphorylation of
IRS-1 , thus preventing IRS-1 degradation and enhancing PI3K activation ... Rapamycin inhibits
S6K1 dependent
IRS-1 serine phosphorylation, increases IRS-1 protein levels, and promotes association of tyrosine phosphorylated IRS-1 with PI3K
Bae et al., Mol Pharmacol 2008
:
An experiment using dominant negative S6K1 supports the essential
role of
S6K1 in the hyperosmolarity stimulated phosphorylation of
IRS1
Glynn et al., Appl Physiol Nutr Metab 2008
(Insulin Resistance) :
Reduced
mTOR/S6K1 signaling during chronic increases in physical activity may
play an important regulatory role in the serine phosphorylation of
IRS-1 , which should be examined as a potential mechanism for attenuation of insulin resistance associated with increased IRS-1 serine phosphorylation
Zhang et al., J Biol Chem 2008
(Insulin Resistance) :
RNAi knockdown demonstrated an important
role for
S6K1 in mediating TNF-alpha induced
IRS-1 inhibition that led to impaired insulin stimulated glucose uptake in adipocytes ... Expression of a dominant negative
S6K1 mutant
prevented TNF induced Ser-270 phosphorylation and
IRS-1 protein degradation
Mayer et al., Endocrinology 2010
:
Insulin phosphorylation of
S6K1 correlated with IRS-1 ser1101 phosphorylation and the mTOR-S6K1 pathway inhibitor rapamycin
prevented IRS-1 serine phosphorylation ... Thus, a sustained elevation of insulin levels diminishes neuronal insulin signaling through
mTOR-S6K1 mediated
IRS-1 serine phosphorylation, proteasomal degradation of IRS-1 and lysosomal degradation of the IR
Xu et al., J Biol Chem 2012
:
Recent work has implicated a role for cullin-RING E3 ubiquitin ligase 7 ( CRL7 ) in targeting
IRS1 for
mTORC1/S6K1 dependent degradation