Gene interactions and pathways from curated databases and text-mining

◀ Back to EPHB2

EPHB2 — GPER1

Text-mined interactions from Literome

Ahola et al., Eur J Biochem 2002 (Breast Neoplasms) : The regulation of GPR30 was independent of ERK pathway activation, but the p38 pathway inhibitor induced GPR30 expression, which suggested a potential gene regulation pathway
Ahola et al., Endocrinology 2002 (Breast Neoplasms) : Transient expression of GPR30 decreased ERK-1 and -2 activity ; and in the cells in which GPR30 expression was decreased by the antisense, ERK activities were increased
Maggiolini et al., J Biol Chem 2004 (Breast Neoplasms) : GPR30 dependent activation of ERK1/2 by E2 and phytoestrogens occurs via a Gbetagamma associated pertussis toxin-sensitive pathway that requires both Src related and EGF receptor tyrosine kinase activities
Park et al., Endocrinology 2009 (Prostatic Hyperplasia) : In normal cells, we found that a nongenomic, rapid E2 signaling pathway is predominantly involved, mediated by G protein coupled receptor-30 and the subsequent activation of ERK1/2
Ding et al., Am J Physiol Cell Physiol 2009 : Estradiol mediated ERK phosphorylation and apoptosis in vascular smooth muscle cells requires GPR 30
Recchia et al., J Biol Chem 2011 (Breast Neoplasms...) : Moreover, we show that HIF-1a-responsive elements located within the promoter region of GPER are involved in hypoxia dependent transcription of GPER , which requires the ROS induced activation of EGFR/ERK signaling in both SkBr3 and HL-1 and cells
Sharma et al., Endocrinology 2011 : GPER is expressed in MIN6 cells, where estradiol and the GPER-selective agonist G-1 mediate calcium mobilization and activation of ERK and phosphatidylinositol 3-kinase ... Our results indicate that GPER activation of the epidermal growth factor receptor and ERK in response to estradiol treatment plays a critical role in the secretion of insulin from ß-cells
Lappano et al., Breast Cancer Res 2012 (Breast Neoplasms...) : Moreover, GPER was required for epidermal growth factor receptor (EGFR) and ERK activation by EGF as ascertained by using MIBE and performing gene silencing experiments