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IGF1 — STAT3
Text-mined interactions from Literome
Takahashi et al., Circ Res 1999
:
These results indicated that ( 1 ) IGF-1 activated JAK1 but not JAK2 or Tyk2 in rat cardiomyocytes ; ( 2 )
IGF-1 induced both tyrosine and serine phosphorylation of STAT1 and STAT3 ; and ( 3 ) the tyrosine phosphorylation of
STAT3 was not caused by JAK1 alone, and protein kinase C and intracellular Ca ( 2+ ) were required for phosphorylation
Zong et al., J Biol Chem 2000
:
We found that
STAT3 , but not STAT5, was activated in
response to
IGF-I in 293T cells cotransfected with IGF-IR and STAT expression vectors ... Dominant negative JAK1 or JAK2 was able to block the
IGF-IR mediated tyrosine phosphorylation of
STAT3 in 293T cells ... A newly identified family of proteins called SOCS ( suppressor of cytokine signaling ), including SOCS1, SOCS2, SOCS3 and CIS, was able to inhibit the
IGF-I induced
STAT3 activation as well with varying degrees of potency, in which SOCS1 and SOCS3 appeared to have the higher inhibitory ability
Zhang et al., Mol Cell Biol 2006
:
Overexpression or downregulation of RACK1 greatly enhances or decreases, respectively,
IR/IGF-1R mediated
activation of
STAT3 and its target gene expression
Ray et al., Int J Oncol 2007
(Breast Neoplasms...) :
MCF-7 cells expressed higher levels of Ob-Rb, Jak2, PI3K,
Stat3 and p-Stat3 in a dose dependent manner to 50 ng/ml at 24 h ; and
IGF-IRalpha increased at 24 h. Cyclin D1 and Cox-2 levels increased with leptin treatment
Jaquish et al., Carcinogenesis 2011
(Pancreatic Neoplasms) :
In pancreatic cancer cells, unlike childhood sarcoma,
STAT-3 , rather than RPS6, is activated in
response to
IGF-1 , in a RON dependent manner
Dal Monte et al., Exp Eye Res 2013
(Disease Models, Animal...) :
Propranolol ophthalmic solutions reduced VEGF and
IGF-1 up-regulation in response to hypoxia and drastically
inhibited HIF-1a accumulation and
STAT3 phosphorylation