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SETD2 — TP53
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Choi et al., J Biochem Mol Biol 2003
(Cell Transformation, Neoplastic...) :
It was recently reported that HIF-1alpha binds a co-activator of the AP-1 transcription factor, Jab-1, which inhibits the
p53 dependent degradation of
HIF-1 and enhances the transcriptional activity of HIF-1 and the subsequent VEGF expression under hypoxic conditions
Schmid et al., Biochem J 2004
(Carcinoma...) :
In addition, low
p53 expression
repressed HIF-1 transactivation without affecting HIF-1alpha protein amount ... We conclude that low
p53 expression
attenuates HIF-1 transactivation by competing for p300, whereas high p53 expression destroys the HIF-1alpha protein and thereby eliminates HIF-1 reporter activity
Sohda et al., Int J Cancer 2004
(Esophageal Neoplasms...) :
Previous reports have suggested that the regulation of
p53 and p21 is
HIF-1 dependent
Vleugel et al., Hum Pathol 2006
(Breast Neoplasms...) :
Transcriptional activity of
HIF-1 may be
repressed by
p53 through competition for transcriptional coactivators such as p300 ... This underlines the importance of p300 levels and
p53 accumulation in the
HIF-1 regulated response toward hypoxia
Hubert et al., J Cell Sci 2006
(Carcinoma, Hepatocellular...) :
Ectopic overexpression of
p53 also
led to an inhibition of
HIF-1 activity
Sano et al., Nature 2007
(Cardiac Output, Low...) :
p53 induced inhibition of
Hif-1 causes cardiac dysfunction during pressure overload
Sano et al., Nihon rinsho. Japanese journal of clinical medicine 2008
(Cardiomegaly...) :
Cardiac angiogenesis played an important role in the maintenance of cardiac function as well as the development of cardiac hypertrophy induced by pressure-overload, and upregulated
p53 induced the transition from cardiac hypertrophy to heart failure through the suppression of
hypoxia inducible factor-1(HIF-1) , which regulates angiogenesis in the hypertrophied heart
Oda et al., PloS one 2008
:
MIF regulates
HIF-1 activity in a
p53 dependent manner
Xie et al., Cell Signal 2008
:
Here we show that
SETD2 could interact with p53 and selectively
regulate the transcription factor activity of
p53
Hiwatashi et al., Anticancer Res 2009
(Anoxia) :
Moreover, the
p53 suppression
induced by
HIF-1a may lead to malignant potential in RAGE transfected Cos7 cells
Yoshioka et al., J Surg Res 2012
(Neovascularization, Pathologic...) :
During hypoxia,
p53 is
stabilized by interaction with
hypoxia-inducible factor-1 (HIF-1) ... Here, we showed that expression of wild-type p53, but not null or mutated
p53 , significantly
suppressed HIF-1 activity and production of VEGF, which mostly depends on the HIF-1ß protein level
de Lange et al., Oncogene 2012
(Anoxia...) :
Also Topotecan, alone or in combination with Nutlin-3, reduced HIF-1a protein levels, suggesting that a certain level of DNA damage response is required for
p53 mediated downregulation of
HIF-1a
Kojima et al., Blood 2011
(Leukemia, Myeloid, Acute) :
p53 activation by Nutlin-3a was not cytotoxic to stromal cells, but reduced CXCL12 mRNA levels and secretion of CXCL12 partially through
p53 mediated
HIF-1a down-regulation
Park et al., Mol Carcinog 2012
(Colonic Neoplasms...) :
HFD feeding increased tumor tissue levels of Ki67, cyclin A, cyclin D1, CDK2, Bcl-xL, and Bcl-2 ; reduced
p53 levels and TUNEL positive apoptotic cells ; increased the levels of CD45, CD68, CD31, VEGF, P-VEGF receptor-2, iNOS, and COX-2 as well as hemoglobin content ; and
increased the levels of
HIF-1a , P-STAT3-Y705, P-STAT3-S727, P-I?B-a, P-p65, p65, P-c-Jun, P-Akt, P-ERK1/2, P-p38, and P-SAPK/JNK
Farhang Ghahremani et al., Cell Death Differ 2013
(Anoxia...) :
Unexpectedly, and for the first time, we demonstrate that
p53 rapidly induces VEGF transcription upon hypoxia exposure by binding, in an
HIF-1a dependent manner, to a highly conserved and functional p53 binding site within the VEGF promoter
Lee et al., J Biol Chem 2013
(Colonic Neoplasms) :
These results identify KLF5 as a transactivator of HIF-1a and show that LPA
regulates HIF-1a by dynamically modulating its interaction with KLF5 and
p53