◀ Back to STAT3
ESR1 — STAT3
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Ciana et al., J Biol Chem 2003
(Neuroblastoma) :
Based on the data presented, we hypothesized that in the presence of prothymosin alpha,
ER alpha activates its direct target genes and increases cell proliferation, whereas in the presence of high levels of TGF-alpha, ER alpha preferentially interacts with
Stat3 and causes cell differentiation
Binai et al., Int J Cancer 2010
(Breast Neoplasms) :
Upon leptin binding to its receptor Ob-RL ( obesity receptor ),
STAT3 tyrosine phosphorylation and transactivation activity were
enhanced by simultaneously expressing
ERalpha ... Interestingly, leptin mediated STAT3 activation was unaffected by co-stimulation with the ERalpha ligands estradiol ( E2 ) or estrogen antagonists ICI182,780 and tamoxifen, implying that enhancement of leptin mediated
STAT3 activity is
independent of
ERalpha ligands
Kinouchi et al., Stroke 2012
(Brain Ischemia...) :
Whether the increase in
p-STAT3 by estrogen is
mediated by the
estrogen receptor a is also obscure
Lee et al., Proc Natl Acad Sci U S A 2012
:
Furthermore, reduction of acetylated
STAT3 in triple negative breast cancer cells
leads to demethylation and activation of the
estrogen receptor-a gene, sensitizing the tumor cells to antiestrogens