◀ Back to PRDX2
ESR1 — PRDX2
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Margueron et al., J Mol Endocrinol 2004
(Breast Neoplasms) :
The
TSA dependent decrease of
ERalpha expression is required to induce the agonist switch of OHTam properties as it is lost in cells constitutively expressing exogenous receptors ( MELN-ERalpha or ERbeta )
Pryzbylkowski et al., Breast Cancer Res Treat 2008
(Breast Neoplasms) :
Trichostatin A (TSA) and 5-Aza 2'deoxycytidine ( AZA ), two well characterized pharmacologic inhibitors of histone deacetylation and DNA methylation,
affect estrogen receptor alpha ( ER ) levels differently in ER-positive versus ER-negative breast cancer cell lines
Fan et al., J Cancer Res Clin Oncol 2008
(Breast Neoplasms) :
It is reported that
ER alpha was
induced in ER alpha negative breast cancer cells by both DNA methyltransferase-1 (DNMT1) inhibitor 5-aza-2'-deoxycytidine ( AZA ) and histone deacetylase (HDAC) inhibitor
trichostatin A (TSA)
Kim et al., Breast Cancer Res 2010
:
Although several previous studies have demonstrated the
role of
TSA in regulation of
estrogen receptor alpha (ERalpha) , the precise mechanism by which TSA affects ERalpha activity remains unclear ... Knockdown of p300 by RNA interference decreased acetylation as well as the protein level of ERalpha, indicating that p300 mediated the
TSA induced stabilization of
ERalpha
Urbinati et al., Int J Pharm 2010
(Breast Neoplasms) :
In MCF-7 cells,
TSA and PXD were efficient
inducers of proteasome mediated
estradiol receptor alpha degradation and they both affected estradiol induced transcription ( TSA > PXD ) contrary to CG