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INS — STAT5B
Text-mined interactions from Literome
Storz et al., Anal Biochem 1999
:
We show in Rat1 fibroblasts stably overexpressing the human IR ( Rat1-HIR-cl5 ) an
insulin dependent direct association and phosphorylation of
STAT5b by IR kinase
Storz et al., FEBS Lett 1999
(Rhabdomyosarcoma) :
Insulin selectively
activates STAT5b , but not STAT5a, via a JAK2 independent signalling pathway in Kym-1 rhabdomyosarcoma cells ... We here describe the selective tyrosine phosphorylation of
STAT5b in Kym-1 cells in
response to
insulin ... Blocking
insulin signalling by HNMPA- ( AM ) ( 3 ), an insulin receptor kinase inhibitor,
resulted in the loss of insulin induced
STAT5b tyrosine phosphorylation, whereas the inhibition of JAK2 by the JAK selective inhibitor tyrphostin AG490 had no effect
Emanuelli et al., J Biol Chem 2000
:
Once induced, SOCS-3 inhibits
insulin activation of
Stat5B without modifying the insulin receptor tyrosine kinase activity ... By inhibiting
insulin stimulated
Stat5B , SOCS-3 appears to function as a negative regulator of insulin signaling
Sawka-Verhelle et al., Endocrinology 2000
(Carcinoma, Hepatocellular...) :
Firstly, we show that both
insulin and insulin-like growth factor I
lead to tyrosine phosphorylation of
Stat 5B , and this promotes binding of the transcription factor to the beta-casein promoter containing a Stat 5 binding site ...
Activation of
Stat 5B by
insulin appears to be Jak2 independent, whereas Jak2 is required for GH-induced Stat 5B activation ... Hence the pathway by which
Stat 5B is
activated by
insulin is different from that used by GH ... In addition, by using Jak1- and Tyk2-deficient cells we exclude the involvement of both Jak1 and Tyk2 in
Stat 5B activation by
insulin
Carvalheira et al., Biol Chem 2003
:
Acutely injected
insulin stimulated a mild increase in tyrosine phosphorylation of JAK2, STAT3 and
STAT5b
Chen et al., Proc Natl Acad Sci U S A 1997
:
Insulin stimulates tyrosine phosphorylation of overexpressed
Stat5b-Ct and endogenous Stat5 in cells overexpressing IR