ArticleMolecular endocrinology (Baltimore, Md.)2006
Bip is a molecular link between the phase I and phase II estrogenic responses in uterus.
Article in Molecular endocrinology (Baltimore, Md.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Heat Shock Proteins and Their Role in Pregnancy: Redefining the Function of "Old Rum in a New Bottle".Frontiers in cell and developmental biology · 2021Review
- The Interplay between Glucose-Regulated Protein 78 (GRP78) and Steroids in the Reproductive System.International journal of molecular sciences · 2018Review
- Endoplasmic Reticulum Stress and Homeostasis in Reproductive Physiology and Pathology.International journal of molecular sciences · 2017Review
- Mechanisms of uterine estrogen signaling during early pregnancy in mice: an update.Journal of molecular endocrinology · 2016Review
- Intraperitoneal Fat through GRP78: A Risk Factor for Endometrial Cancer.Analytical cellular pathology (Amsterdam) · 2016Article
- Article
- GRP78 expression and regulation in the mouse uterus during embryo implantation.Journal of molecular histology · 2014Article
- The endoplasmic reticulum stress marker, glucose-regulated protein-78 (GRP78) in visceral adipocytes predicts endometrial cancer progression and patient survival.Gynecologic oncology · 2013Article
- KLF15 negatively regulates estrogen-induced epithelial cell proliferation by inhibition of DNA replication licensing.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Nucleolar Sik-similar protein (Sik-SP) is required for the maintenance of uterine estrogen signaling mechanism via ERα.Molecular endocrinology (Baltimore, Md.) · 2012Article
- Mouse primary uterine cell coculture system revisited: ovarian hormones mimic the aspects of in vivo uterine cell proliferation.Endocrinology · 2011Article
- GPR30 activation opposes estrogen-dependent uterine growth via inhibition of stromal ERK1/2 and estrogen receptor alpha (ERα) phosphorylation signals.Endocrinology · 2011Article
- Diarylheptanoid phytoestrogens isolated from the medicinal plant Curcuma comosa: biologic actions in vitro and in vivo indicate estrogen receptor-dependent mechanisms.Environmental health perspectives · 2009Article
- Cooperative control via lymphoid enhancer factor 1/T cell factor 3 and estrogen receptor-alpha for uterine gene regulation by estrogen.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Increased level of cellular Bip critically determines estrogenic potency for a xenoestrogen kepone in the mouse uterus.Endocrinology · 2007Article
- Chromatin immunoprecipitation assay detects ERalpha recruitment to gene specific promoters in uterus.Biological procedures online · 2006Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Uterine estrogenic actions are biphasic, early (phase I) and late (phase II) responses. However, the molecular linkage between these phases is not known. Although certain phase I responses are considered estrogen receptor (ER)alpha and ERbeta independent, the phase II responses are ERalpha dependent. We previously observed that among several genes Bip is induced by estrogen in the mouse uterus in an ER-independent manner as a phase I response. Bip is a member of the chaperone family and plays roles in protein processing and confers cellular protection. However, its role in estrogen-dependent uterine biology is unknown. We show here a new function of Bip in regulating estrogen signaling in the uterus. Bip, induced during the phase I responses, molecularly interacts with ERalpha required for estrogen-mediated phase II growth responses. Utilizing in vivo and in vitro model systems, we found that adenovirus-driven suppression of Bip antagonizes ERalpha-mediated uterine gene transcription. Importantly, down-regulation of Bip compromises estrogen-dependent phase II growth responses with sustained phase I responses. In conclusion, Bip is critical for coordinating estrogen-elicited biphasic responses and serves as a molecular link between ERalpha-independent and -dependent estrogenic responses in the uterus.
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