Gene interactions and pathways from curated databases and text-mining

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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