Gene interactions and pathways from curated databases and text-mining

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HIF1A — TP53

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

Ravi et al., Genes Dev 2000 (Adenocarcinoma...) : Loss of p53 in tumor cells enhances HIF-1alpha levels and augments HIF-1 dependent transcriptional activation of the vascular endothelial growth factor ( VEGF ) gene in response to hypoxia
Suzuki et al., Oncogene 2001 : Depletion of the dephosphorylated HIF-1alpha , by using the Hsp90 inhibitor geldanamycin A that had little effect on the phosphorylated HIF-1alpha expression, suppressed p53 induction and subsequent apoptosis
Chen et al., J Biol Chem 2003 (Anoxia) : These results have significant implications regarding the molecular mechanism by which p53 is activated by HIF-1 alpha in response to hypoxia
Kaluzová et al., Mol Cell Biol 2004 (Anoxia) : DNA damage is a prerequisite for p53 mediated proteasomal degradation of HIF-1alpha in hypoxic cells and downregulation of the hypoxia marker carbonic anhydrase IX ... The activated p53 mediated increased proteasomal degradation of HIF-1alpha protein, resulting in considerably lower steady-state levels of HIF-1alpha protein in hypoxic MCF-7 cells but not in Saos-2 cells
Demidenko et al., Oncogene 2005 : Under normoxia, while inducing p53 , inhibitors of transcription did not induce HIF-1alpha
Larsen et al., Adv Exp Med Biol 2005 (Neoplasms) : Moreover, p53 is stabilized by binding to HIF-1alpha , whereas its interaction with Jab1 targets p53 for degradation
Calvert et al., J Appl Physiol 2006 (Brain Ischemia...) : An increase in the dephosphorylated form of HIF-1alpha was followed by an increase in the association of HIF-1alpha with p53 and an increase in p53 levels
Achison et al., Oncogene 2007 (Neoplasms) : p53 is not required , however, for the rimcazole induced engagement of HIF-1alpha in proapoptotic mode as HIF-1alpha knockdown attenuates rimcazole induced death to comparable extents in p53 mutant and wild-type cell systems
Koh et al., Mol Cancer Ther 2008 : Studies of the mechanism of PX-478 action showed that HIF-1alpha inhibition occurs in both normoxia and hypoxia and does not require pVHL or p53
Bove et al., J Biol Chem 2008 (Inflammation) : Finally, NO-mediated inhibition of cell migration was associated with HIF-1alpha dependent induction of PAI-1 and activation of p53 , both negative regulators of epithelial cell migration
Yang et al., Mol Cell Biol 2009 : Here, we show that induction of p53 by the small-molecule RITA ( reactivation of p53 and induction of tumor cell apoptosis ) [ 2,5-bis ( 5-hydroxymethyl-2-thienyl ) furan ] ( NSC-652287 ) inhibits HIF-1alpha and vascular endothelial growth factor expression in vivo and induces significant tumor cell apoptosis in normoxia and hypoxia in p53 positive cells
Choy et al., J Cell Physiol 2010 (Cardiomegaly...) : PKB/Akt activation inhibits p53 mediated HIF1A degradation that is independent of MDM2 ... In that context, p53 induces HIF1A degradation which in turn provokes the transition from compensatory hypertrophy to myocardial thinning and chamber dilatation ( Sano et al., 2007, Nature 446 : 444-448 ) ... In order to investigate the mechanism of p53 induced HIF1A degradation, we used the established in vitro model of deferroxamine ( DFX ) -induced HIF1A accumulation in H9c2 cardiac cells ( Sano et al., 2007, Nature 446 : 444-448 ) ... In summary, we propose that p53 induced HIF1A degradation is not exclusively MDM2 mediated, but reversible by PKB/Akt phosphorylation
Lou et al., PloS one 2010 : Camptothecin is a reported inhibitor of HIF-1alpha translation, while mitomycin C has been reported to induce p53 dependent HIF-1alpha degradation ... In this study we demonstrate that the inhibitory effect of mitomycin C on HIF-1alpha protein expression is not dependent on p53 and protein degradation, but also involves HIF-1alpha translational regulation
Rohwer et al., PloS one 2010 (Stomach Neoplasms) : HIF-1alpha markedly suppressed chemotherapy induced activation of p53 and p21 as well as the retinoblastoma protein, eventually resulting in cell cycle arrest ... Reduced formation of reactive oxygen species in HIF-1alpha-competent cells was identified as the molecular mechanism of HIF-1alpha mediated inhibition of p53 ... Furthermore, loss of HIF-1alpha abrogated, in a p53 dependent manner, chemotherapy induced DNA binding of NF-kappaB and expression of anti-apoptotic NF-kappaB target genes