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ESR2 — IGF1

Text-mined interactions from Literome

Campagnoli et al., Gynecol Endocrinol 1999 (Breast Neoplasms...) : Actually, estrogens and IGF-I have a synergistic effect on cell proliferation, and IGF-I is necessary for maximum estrogen-receptor activation in breast cancer cell lines
Richards et al., Mol Endocrinol 2002 : Furthermore, E2 enhances expression of other IGF-I pathway components ( IGF-1Rbeta and Glut-1 ), and IGF-I enhances expression of ERbeta , indicating that these two hormones comprise an autocrine regulatory network within growing follicles
Martin et al., J Nutr 2002 (Breast Neoplasms) : Recent studies show that the effects of IGF-I on estrogen receptor activity are mediated in part by the protein kinase A and phosphatidylinositol-3-kinase/Akt pathways
Seidlova-Wuttke et al., Eur J Endocrinol 2003 : While E ( 2 ) stimulated uterine weight and expression of progesterone receptor (PR), the complement protein ( C3 ) and IGF-I genes, and inhibited gene expression of the estrogen receptor beta (ERbeta) in the uterus, no such effect was observed under acute CR treatment
Maor et al., J Endocrinol 2006 (Breast Neoplasms) : The aim of our study was to examine the transcriptional mechanisms involved in regulation of IGF-IR gene expression by the estrogen receptor ( ER )
Hewitt et al., J Biol Chem 2010 : This proliferation and IGF1 synthesis requires the estrogen receptor ( ER ) , which binds directly to target DNA sequences ( estrogen-responsive elements or EREs ), or interacts with other transcription factors, such as AP1, to impact transcription
Lee et al., Biomed Pharmacother 1995 (Breast Neoplasms) : In addition, recent data now indicate that IGF ligands can also activate estrogen receptor ( ER ) in a ligand independent manner
Duenas et al., Neuroscience 1996 : These findings suggest that estradiol induced activation of the estrogen receptor in developing hypothalamic cells requires the presence of insulin-like growth factor-I , and that both estradiol and insulin-like growth factor-I use the estrogen receptor as a mediator of their trophic effects on hypothalamic neurons
García-Segura et al., Horm Res 1996 : These findings indicate that estrogen induced activation of the estrogen receptor in developing hypothalamic neurons requires the presence of IGF-I and that both estradiol and IGF-I use the estrogen receptor to mediate their trophic effects on hypothalamic cells