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ESR1 — 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 *
-
IRef Bind_translation Interaction:
ESR1
—
TP53
(affinity chromatography technology)
Liu et al., Cancer Res 2000*
-
IRef Biogrid Interaction:
ESR1
—
TP53
(physical association, affinity chromatography technology)
Duong et al., Cancer Res 2007*
-
IRef Biogrid Interaction:
ESR1
—
TP53
(direct interaction, pull down)
Liu et al., Cancer Res 2000*
-
MIPS CORUM Er-alpha-p53-hdm2 complex:
Er-alpha-p53-hdm2 complex complex (ESR1-MDM2-TP53)
Liu et al., Cancer Res 2000*
-
IRef Corum Interaction:
Complex of ESR1-MDM2-TP53
(association, pull down)
Liu et al., Cancer Res 2000*
-
IRef Hprd Interaction:
TP53
—
ESR1
(in vitro)
Liu et al., Cancer Res 2000*
-
IRef Ophid Interaction:
ESR1
—
TP53
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
ESR1
—
TP53
(aggregation, confirmational text mining)
Liu et al., Cancer Res 2000*
Text-mined interactions from Literome
Kato et al., J Biol Chem 2002
(Cell Transformation, Neoplastic) :
In addition, overexpression of wild type
ERalpha in NIH3T3 cells
resulted in the significant increase in the MDM2 protein level and the resultant suppression of
p53 transcriptional activity
Angeloni et al., J Endocrinol 2004
(Breast Neoplasms) :
Regulation of
estrogen receptor-alpha expression by the tumor suppressor gene
p53 in MCF-7 cells ... The results presented here demonstrate that
p53 upregulates
estrogen receptor-alpha (ER alpha) expression in the human breast cancer cell line MCF-7 ... In the stable clones, expression of antisense
p53 resulted in a decrease in the expression of
ER alpha protein ... To determine whether the
effects of
p53 on the expression of
ER alpha were due to changes in transcription, deletion mutants of the ER alpha promoter were used ... This experimental approach demonstrated that p53 up-regulates ER alpha gene expression by increasing transcription of the gene through elements located upstream of promoter A. Transfection assays using p53 mutants further demonstrated that the
p53 induced increase in
ER alpha gene transcription was not dependent on the ability of p53 to bind to DNA but on its ability to interact with other proteins
Sayeed et al., Cancer Res 2007
(Bone Neoplasms...) :
Transcriptional derepression of Survivin by ERalpha is dependent on the p53 binding site on the Survivin promoter, consistent with our observation that
p53 is
necessary for
ERalpha to access the promoters
Liu et al., Breast Cancer Res Treat 2009
(Breast Neoplasms) :
These findings suggest that alleviating the inhibitory
effect of
ERalpha on
p53 could be one of the molecular mechanisms underlying activation of p53 by radiation in breast tumors, and therefore, could be exploited to develop more effective ways of combining radiation therapy with systemic therapies such as hormonal therapy and chemotherapy
Shirley et al., Cancer Res 2009
(Breast Neoplasms) :
Transcriptional
regulation of
estrogen receptor-alpha by
p53 in human breast cancer cells
Seifert et al., Int J Oncol 2009
(Breast Neoplasms) :
TCDD mediates inhibition of
p53 and
activation of
ERalpha signaling in MCF-7 cells at moderate hypoxic conditions
Menendez et al., Proc Natl Acad Sci U S A 2010
(Neoplasms) :
Estrogen receptor acting in cis
enhances WT and mutant
p53 transactivation at canonical and noncanonical p53 target sequences
Rasti et al., Pathol Oncol Res 2012
(Breast Neoplasms) :
To investigate the mechanism of
ESR1 gene
regulation by
p53 , chromatin immunoprecipitation was applied to assess the binding of p53, DNMT1, HDAC1 and MeCP2 to both silenced ESR1 promoter in MDA-MB-468 cells and active ESR1 promoter in MCF-7 breast cancer cells