D
Dennis B. Lubahn
Researcher at University of Missouri
Publications - 201
Citations - 29869
Dennis B. Lubahn is an academic researcher from University of Missouri. The author has contributed to research in topics: Estrogen receptor & Estrogen receptor alpha. The author has an hindex of 79, co-authored 200 publications receiving 28809 citations. Previous affiliations of Dennis B. Lubahn include Mayo Clinic & University of Missouri System.
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Journal ArticleDOI
Estrogen Inhibits Cardiac Hypertrophy: Role of Estrogen Receptor-β to Inhibit Calcineurin
Ali Pedram,Mahnaz Razandi,Dennis B. Lubahn,Jinghua Liu,Mani A. Vannan,Ellis R. Levin,Ellis R. Levin +6 more
TL;DR: E2 acting mainly through ERbeta mitigates the important signaling by AngII that produces cardiac hypertrophy and fibrosis in female mice and substantially prevented ventricular interstitial cardiac fibrosis as induced by Ang II.
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Intraovarian actions of oestrogen
TL;DR: Microarray technologies, combined with specific hormone treatment regimens are likely to provide an attractive, alternative approach to using mutant mice in clarifying the direct actions of oestrogen in the ovaries of other species.
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Paracrine Regulation of Epithelial Progesterone Receptor by Estradiol in the Mouse Female Reproductive Tract
TL;DR: Analysis of estrogen receptor alpha (ERalpha) knockout mice showed that ERalpha is essential for E(2))-induced PR expression in both vaginal epithelium and stroma, and for E (2)-induced down-regulation, but not constitutive expression of PR in uterine epithelia.
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Role of stromal and epithelial estrogen receptors in vaginal epithelial proliferation, stratification, and cornification.
David L. Buchanan,Takeshi Kurita,Julia A. Taylor,Dennis B. Lubahn,Gerald R. Cunha,Paul S. Cooke +5 more
TL;DR: E2-induced vaginal epithelial proliferation is mediated indirectly through stromal ER alpha, consistent with the recent findings in uterus, and the first known functions attributed to epithelial ER alpha in vivo are attributed.
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Estrogen receptor-beta prevents cardiac fibrosis.
TL;DR: The results establish the cardiac fibroblast as an important target for hypertrophic/fibrosis-inducing peptides the actions of which were mitigated by E2/ERβ acting in these stromal cells.