Gene interactions and pathways from curated databases and text-mining

◀ Back to HIF1A

HIF1A — STAT3

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

Jung et al., FASEB J 2005 (Ischemia...) : Interestingly, activated STAT3 increased HIF-1alpha protein levels due to the HIF-1alpha stability by blocking HIF-1alpha degradation and accelerated its de novo synthesis
Jeong et al., J Biol Chem 2007 : Our findings collectively suggest that hypoxia induced in vitro differentiation of mESCs is triggered, at least in part, by the HIF-1alpha mediated suppression of LIF-STAT3 signaling
Niu et al., Mol Cancer Res 2008 : Additionally, Stat3 activity in the nontransformed cells in the tumor milieu affects HIF-1alpha RNA expression of the entire growing tumor ... Consistent with a role of Stat3 in regulating HIF-1alpha RNA transcription, elevated Stat3 activity increases HIF-1alpha promoter activity, and Stat3 protein binds to the HIF-1alpha promoter in both transformed cells and in growing tumors
Noman et al., J Immunol 2009 (Anoxia...) : Interestingly, gene silencing of STAT3 by small interfering RNA resulted in HIF-1alpha inhibition and a significant restoration of target cell susceptibility to CTL induced killing under hypoxic conditions by a mechanism involving at least in part down-regulation of AKT phosphorylation
Wincewicz et al., Folia Histochem Cytobiol 2009 (Breast Neoplasms...) : STAT3 and hypoxia induced proteins -- HIF-1alpha , EPO and EPOR in relation with Bax and Bcl-xL in nodal metastases of ductal breast cancers
Cascio et al., J Cell Physiol 2010 (Breast Neoplasms) : In addition, using siRNA knockdown, we demonstrated that the presence of STAT3 is necessary for CoCl ( 2 ) -mediated HIF-1 alpha nuclear accumulation and recruitment on VEGF promoter