Gene interactions and pathways from curated databases and text-mining

◀ Back to ESR1

ESR1 — STAT5A

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

Stoecklin et al., J Steroid Biochem Mol Biol 1999 : The estrogen receptor diminishes Stat5 mediated induction and the androgen receptor has no effect ... Conversely, Stat5 negatively interferes with glucocorticoid receptor, mineralocorticoid receptor and progesterone receptor induced transcription from the MMTV LTR and the estrogen receptor induced transcription from an ERE containing promoter
Frasor et al., Mol Endocrinol 2001 : Interestingly, either Stat5a or Stat5b could stimulate ERalpha transcription while stimulation of ERbeta occurred only in the presence of Stat5b ... These findings indicate that PRL stimulation of ER expression occurs at the level of transcription and that PRL regulation of ERalpha can be mediated by either Stat5a or Stat5b, while regulation of ERbeta appears to be mediated only by Stat5b
Yamashita et al., Oncogene 2003 : Cotransfection experiments revealed that Stat5aDelta740 completely blocked transcriptional activity of endogenous estrogen receptor in T47D and MCF7 cells, and of both ER alpha and ER beta in COS-7 cells ... Cotransfection experiments revealed that Stat5aDelta740 completely blocked transcriptional activity of endogenous estrogen receptor in T47D and MCF7 cells, and of both ER alpha and ER beta in COS-7 cells
Frasor et al., Trends Endocrinol Metab 2003 : A single nucleotide difference between these two response elements is responsible for the observation that either Stat5a or Stat5b can stimulate Esr1 transcription, whereas only Stat5b can activate transcription of Esr2
Boerner et al., Mol Endocrinol 2005 (Breast Neoplasms) : ERalpha transcriptional activity was not necessary for suppression of STAT5 activity ... However, ERalpha did prevent basal increases in STAT5 activity with overexpressed c-Src