Search Results
Search for other papers by Atsushi Fukushima in
Google Scholar
PubMed
Search for other papers by Ping Yin in
Google Scholar
PubMed
Search for other papers by Maho Ishida in
Google Scholar
PubMed
Search for other papers by Nobuhiro Sugiyama in
Google Scholar
PubMed
Search for other papers by Jun Arita in
Google Scholar
PubMed
Introduction The preovulatory surge of luteinizing hormone (LH) secretion in cyclic rats and the daily surge in ovariectomized, estrogen-treated rats are caused by the central action of estrogen on the gonadotropin-releasing hormone
Search for other papers by Soyoung Choi in
Google Scholar
PubMed
Search for other papers by Hyejin Shin in
Google Scholar
PubMed
Search for other papers by Haengseok Song in
Google Scholar
PubMed
Search for other papers by Hyunjung Jade Lim in
Google Scholar
PubMed
blood vessels. Many uterine functions are under the regulation of ovarian steroid hormones, estrogens and progesterone (P 4 ; Dey et al . 2004 , Das 2009 ), and uterine cell types respond to hormones in a differential manner. Ovarian estrogen targets
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Beverly A S Reyes in
Google Scholar
PubMed
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Hiroko Tsukamura in
Google Scholar
PubMed
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Helen I’Anson in
Google Scholar
PubMed
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Maria Amelita C Estacio in
Google Scholar
PubMed
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Kanjun Hirunagi in
Google Scholar
PubMed
Department of Neurosurgery, Farber Institute for Neurosciences, Thomas Jefferson University, 900 Walnut Street, Suite 400, Philadelphia, Pennsylvania 19107, USA
Department of Biology, Washington and Lee University, Lexington, Virginia 24450-03, USA
Search for other papers by Kei-Ichiro Maeda in
Google Scholar
PubMed
investigations have shown that 48-h fasting dramatically suppresses pulsatile luteinizing hormone (LH) secretion in female rats, and the suppression is largely dependent on the estrogenic milieu ( Cagampang et al. 1991 , Maeda et al. 1996 ). As such, 48-h
Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of
Search for other papers by Melyssa R Bratton in
Google Scholar
PubMed
Search for other papers by James W Antoon in
Google Scholar
PubMed
Search for other papers by Bich N Duong in
Google Scholar
PubMed
Search for other papers by Daniel E Frigo in
Google Scholar
PubMed
Section of Hematology and Medical Oncology, Structural and Cellular Biology, Department of Medical Genetics, Center for Nuclear Receptors and Cell Signaling, Department of Medicine, Tulane University, 1430 Tulane Avenue, SL-78, New Orleans, Louisiana 70112, USA Departments of
Search for other papers by Syreeta Tilghman in
Google Scholar
PubMed
Search for other papers by Bridgette M Collins-Burow in
Google Scholar
PubMed
Search for other papers by Steven Elliott in
Google Scholar
PubMed
Search for other papers by Yan Tang in
Google Scholar
PubMed
Search for other papers by Lilia I Melnik in
Google Scholar
PubMed
Search for other papers by Ling Lai in
Google Scholar
PubMed
Search for other papers by Jawed Alam in
Google Scholar
PubMed
Search for other papers by Barbara S Beckman in
Google Scholar
PubMed
Search for other papers by Steven M Hill in
Google Scholar
PubMed
Search for other papers by Brian G Rowan in
Google Scholar
PubMed
Search for other papers by John A McLachlan in
Google Scholar
PubMed
Search for other papers by Matthew E Burow in
Google Scholar
PubMed
Introduction Various agents regulate estrogen receptor α (ERα) activity in addition to 17β-estradiol (E 2 ), including peptide growth factors (PGFs) such as epidermal growth factor (EGF) and insulin-like growth factor 1 (IGF1; Ignar-Trowbridge et
Search for other papers by Annica Andersson in
Google Scholar
PubMed
Search for other papers by Anna E Törnqvist in
Google Scholar
PubMed
Search for other papers by Sofia Moverare-Skrtic in
Google Scholar
PubMed
Search for other papers by Angelina I Bernardi in
Google Scholar
PubMed
Search for other papers by Helen H Farman in
Google Scholar
PubMed
Search for other papers by Pierre Chambon in
Google Scholar
PubMed
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Search for other papers by Cecilia Engdahl in
Google Scholar
PubMed
Search for other papers by Marie K Lagerquist in
Google Scholar
PubMed
Search for other papers by Sara H Windahl in
Google Scholar
PubMed
Search for other papers by Hans Carlsten in
Google Scholar
PubMed
Search for other papers by Claes Ohlsson in
Google Scholar
PubMed
Search for other papers by Ulrika Islander in
Google Scholar
PubMed
Introduction Besides the major roles of estrogens in reproduction and bone health, estrogens have strong impact on the immune system ( Straub 2007 ). In general, estrogens inhibit thymus size and hamper T and B lymphopoiesis, in thymus and
Department of Reproductive Biology, Department of Reproductive Biology, National Institute of Perinatology and School of Medicine, Universidad Autónoma Metropolitana Iztapalapa, Mexico City P.C. 09340, Mexico
Search for other papers by Ana E Lemus in
Google Scholar
PubMed
Search for other papers by Juana Enríquez in
Google Scholar
PubMed
Search for other papers by Ángeles Hernández in
Google Scholar
PubMed
Search for other papers by René Santillán in
Google Scholar
PubMed
Search for other papers by Gregorio Pérez-Palacios in
Google Scholar
PubMed
et al . 1993 ) and also prevents bone loss in young women treated with LH-releasing agonists ( Riis et al . 1990 ). The mechanisms of estrogen-like bone actions of NET are not fully understood, particularly since this steroid molecule neither
Search for other papers by Ying Chen in
Google Scholar
PubMed
Search for other papers by Kelsey Breen in
Google Scholar
PubMed
Search for other papers by Melissa E Pepling in
Google Scholar
PubMed
breakdown is regulated or coordinated with neonatal development. Recent research has implicated estrogen signaling in the cyst breakdown process. Neonatal exposure to genistein, an estrogen-like compound from soy, induces multiple oocyte follicles (MOFs) in
Search for other papers by Ferran Jardí in
Google Scholar
PubMed
Gerontology and Geriatrics, Department of Chronic Diseases, Metabolism and Ageing (CHROMETA), KU Leuven, Leuven, Belgium
Search for other papers by Michaël R Laurent in
Google Scholar
PubMed
Search for other papers by Vanessa Dubois in
Google Scholar
PubMed
Search for other papers by Nari Kim in
Google Scholar
PubMed
Search for other papers by Rougin Khalil in
Google Scholar
PubMed
Search for other papers by Brigitte Decallonne in
Google Scholar
PubMed
Search for other papers by Dirk Vanderschueren in
Google Scholar
PubMed
Search for other papers by Frank Claessens in
Google Scholar
PubMed
research. Nonetheless, the strongest body of evidence supporting that physical activity is biologically regulated still comes from preclinical studies. Androgens and estrogens are key regulators of reproductive organs but also exert multiple effects on
Search for other papers by C D Simmons in
Google Scholar
PubMed
Search for other papers by J M P Pabona in
Google Scholar
PubMed
Search for other papers by Z Zeng in
Google Scholar
PubMed
Search for other papers by M C Velarde in
Google Scholar
PubMed
Search for other papers by D Gaddy in
Google Scholar
PubMed
Search for other papers by F A Simmen in
Google Scholar
PubMed
Search for other papers by R C M Simmen in
Google Scholar
PubMed
Introduction The steroid hormone 17β-estradiol (E 2 ) regulates numerous physiological and developmental processes in target tissues by binding to its cognate receptors estrogen receptor-α (ESR1) and -β (ESR2) in the presence of numerous co
Search for other papers by F Lucio-Oliveira in
Google Scholar
PubMed
Search for other papers by C R Franci in
Google Scholar
PubMed
of OT mRNA in the magnocellular neurones of the PVN ( Van Tol et al . 1988 ) increases at the onset of puberty and decreases after castration ( Miller et al . 1989 ), suggesting a possible influence of estrogen on OT expression levels. The