Gene interactions and pathways from curated databases and text-mining

◀ Back to STAT1

FGF2 — STAT1

Text-mined interactions from Literome

Sahni et al., Genes Dev 1999 : FGF treatment of RCS cells induces phosphorylation of STAT-1 , its translocation to the nucleus, and an increase in the expression of the cell-cycle inhibitor p21WAF1/CIP1
Huang et al., Oncogene 2002 (Fibrosarcoma...) : In the present study, we used Stat1 knockout tumor cells to determine ( 1 ) whether Stat1 can regulate angiogenesis, growth, and metastasis of tumor cells ; and ( 2 ) whether Stat1 is required for the inhibitory effect of IFN-beta on the expression of angiogenic factor bFGF ... Therefore, Stat1 is essential for IFN mediated inhibition of bFGF production, suggesting that tumor-intrinsic Stat1 is an important mediator for antiangiogenic signals, such as IFN
Zhang et al., Exp Eye Res 2005 : Retinas from embryonic and neonatal stages showed that STAT3 but not STAT1 was activated in response to ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), fibroblast growth factor-1 (FGF1), fibroblast growth factor-2 (FGF2) , epidermal growth factor (EGF), interferon-alpha ( IFN-alpha ) and interferon-gamma (IFN-gamma) in distinct patterns
Krejci et al., J Cell Sci 2008 : However, as demonstrated by western blotting with phosphorylation-specific antibodies, imaging of STAT nuclear translocation, STAT transcription factor assays and STAT luciferase reporter assays, FGF does not activate STAT1 or STAT3 in RCS chondrocytes, which nevertheless respond to a FGF stimulus with potent growth arrest
Krejci et al., Cell Signal 2009 : Despite the accumulation, both endogenous and cytokine induced activation of STAT1 and STAT3 is impaired by FGF , as demonstrated by imaging of active STAT nuclear translocation and analyses of STAT activatory phosphorylation and transcriptional activation
Sundaram et al., Mol Endocrinol 2009 (Osteitis Deformans) : These results suggest STAT-1 is a downstream effector of FGF-2 signaling and that elevated levels of FGF-2 stimulates RANKL expression in PDB
Puhr et al., Endocr Relat Cancer 2010 (Carcinoma...) : In the presence of FGF-2 , neither STAT3, STAT1 , nor Akt could be phosphorylated
Johnson et al., Oncogene 1998 (Breast Neoplasms...) : FGF signaling activates STAT1 and p21 and inhibits the estrogen response and proliferation of MCF-7 cells