Hormone Research

Total Page:16

File Type:pdf, Size:1020Kb

Hormone Research RECENT PROGRESS IN HORMONE RESEARCH Edited by ANTHONY R. MEANS VOLUME 57 Reproductive Hormones & Human Health “Recent Progress in Hormone Research” is an annual publication of The Endocrine Society that is published under the editorial auspices of Endocrine Reviews. The Endocrine Society 4350 East West Highway, Suite 500 Bethesda, Maryland 20814 Copyright 2002 by The Endocrine Society All Rights Reserved The reproduction or utilization of this work in any form or in any electronic, mechanical, or other means, now known or hereafter invented, including photocopying or recording and in any information storage or retrieval system, is forbidden, except as may be expressly permitted by the 1976 Copyright Act or by permission of the publisher. ISBN 0–879225-45-X CONTENTS Senior Author Correspondence Information v 1. Cellular and Molecular Pathways Regulating Mammalian Sex Determination 1 Christopher Tilmann and Blanche Capel 2. Steroidogenic Factor 1: An Essential Mediator of Endocrine Development 19 Keith L. Parker, Douglas A. Rice, Deepak S. Lala, Yayoi Ikeda, Xunrong Luo, Margaret Wong, Marit Bakke, Liping Zhao, Claudia Frigeri, Neil A. Hanley, Nancy Stallings, and Bernard P. Schimmer 3. Molecular Basis of Mammalian Gamete Binding 37 David J. Miller, Xudong Shi, and Heather Burkin 4. Regulation of the Mitotic and Meiotic Cell Cycles in the Male Germ Line 75 Debra J. Wolgemuth, Erika Laurion, and Karen M. Lele 5. Male Germ Cell Gene Expression 103 Edward M. Eddy 6. The Expression of the Follicle-stimulating Hormone Receptor in Spermatogenesis 129 Leslie L. Heckert and Michael D. Griswold 7. Identification of Specific Sites of Hormonal Regulation in Spermatogenesis in Rats, Monkeys, and Man 149 R.I. McLachlan, L. O’Donnell, S.J. Meachem, P.G. Stanton, D.M. de Kretser, K. Pratis, and D.M. Robertson 8. Molecular Defects of the Androgen Receptor 181 Michael J. McPhaul 9. Novel Signaling Pathways That Control Ovarian Follicular Development, Ovulation, and Luteinization 195 JoAnne S. Richards, Darryl L. Russell, Scott Ochsner, Minnie Hsieh, Kari H. Doyle, Allison E. Falender, Yuet K. Lo, and S. Chidananda Sharma 10. Transcription Factors Underlying the Development and Endocrine Functions of the Placenta 221 James C. Cross, Lynn Anson-Cartwright, and Ian C. Scott 11. Neuroendocrine Modulation and Repercussions of Female Reproductive Aging 235 Phyllis M. Wise, Matthew J. Smith, Dena B. Dubal, Melinda E. Wilson, Shane W. Rau, Adrienne B. Cashion, Martina Bo¨ttner, and Katherine L. Rosewell iii iv CONTENTS 12. Hormonal Changes in the Menopause Transition 257 Henry G. Burger, Emma C. Dudley, David M. Robertson, and Lorraine Dennerstein 13. Role of Hormonal and Reproductive Factors in the Etiology and Treatment of Uterine Leiomyoma 277 Cheryl L. Walker 14. Definition of the Molecular and Cellular Mechanisms Underlying the Tissue-selective Agonist/Antagonist Activities of Selective Estrogen Receptor Modulators 295 Donald P. McDonnell, Caroline E. Connor, Ashini Wijayaratne, Ching-yi Chang, and John D. Norris 15. Aromatase and Its Inhibitors: Significance for Breast Cancer Therapy 317 Evan R. Simpson and Mitch Dowsett 16. Reproductive Functions of Progesterone Receptors 339 Orla M. Conneely, Biserka Mulac-Jericevic, Francesco DeMayo, John P. Lydon, and Bert W. O’Malley 17. Estrogen Actions Throughout the Brain 357 Bruce McEwen 18. Sex Steroids and Bone 385 S.C. Manolagas, S. Kousteni, and R.L. Jilka 19. Anabolic Steroids 411 Cynthia M. Kuhn 20. Prolactin Modulation of Immune and Inflammatory Responses 435 Li-yuan Yu-Lee Author Index 457 Subject Index 459 Senior Author Correspondence Information Henry G. Burger James Cross Prince Henry’s Institute of Medical Research Department of Biochemistry & Molecular Level 4, Block E Biology Monash Medical Centre University of Calgary Faculty of Medicine 246 Clayton Road HSC Room 2279 Clayton, Victoria 3168 Australia 3330 Hospital Drive, NW Phone: 011-61-3-9594-3553 Calgary, Alberta T2N 4N1 Canada Fax: 011-61-3-9594-3558 Phone: 403-220-6876 E-mail: [email protected] Fax: 403-270-0737 E-mail: [email protected] Blanche Capel Department of Cell Biology Edward M. Eddy Duke University Medical Center Laboratory of Reproductive and 340 Nanaline Duke Developmental Toxicology Box 3709 National Institute of Environmental Health Durham, NC 27710 Sciences Phone: 919-684-6390 National Institutes of Health Fax: 919-681-7978 111 T.W. Alexander Drive, Building 101, E-mail: [email protected] Room C422a Research Triangle Park, NC 27709-2233 Phone: 919-541-3015 Fax: 919-541-3800 Orla M. Conneely E-mail: [email protected] Department of Molecular and Cellular Biology M-511 Debakey Building Baylor College of Medicine Michael D. Griswold Houston, TX 77030 School of Molecular Biosciences Phone: 713-798-6233 Center for Reproductive Biology E-mail: [email protected] Washington State University 630 Fulmer Hall Pullman, WA 99164-4660 Phone: 509-335-6281 Fax: 509-335-9688 E-mail: [email protected] v vi CORRESPONDENCE INFORMATION Cynthia M. Kuhn Robert I. McLachlan Department of Pharmacology and Cancer Male Reproductive Endocrinology Group Biology Prince Henry’s Institute of Medical Research Duke University Medical Center Level 4, Block E 4011 Bryan Research Building Monash Medical Centre Durham, NC 27710 246 Clayton Road Phone: 919-684-8828 Clayton, Victoria, 3168, Australia Fax: 919-681-8609 Phone: 011-61-3-9594-4372 E-mail: [email protected] Fax: 011-61-3-9594-6125 E-mail: [email protected] S.C. Manolagas Center for Osteoporosis and Metabolic Bone Michael J McPhaul Diseases Department of Internal Medicine Division of Endocrinology and Metabolism Division of Endocrinology and Metabolism University of Arkansas Medical School University of Texas Southwestern Medical 4301 W. Markham Street, Slot 587 Center Little Rock, AR 72205 5323 Harry Hines Boulevard Phone: 501-686-5130 Dallas, Texas 75390-8857 Fax: 501-296-1002 Phone: 214-648-3494 E-mail: [email protected] Fax: 214-648-8917 E-mail: [email protected] Donald P. McDonnell Department of Pharmacology and Cancer Biology David J Miller Duke University Medical Center Department of Animal Sciences Box 3813 University of Illinois at Urbana-Champaign Levine Science Research Center, C259 328 Animal Sciences Laboratory Research Drive 1207 West Gregory Drive Durham, NC 27710 Urbana, Illinois 61801 Phone: 919-684-6035 Phone: 217-333-3408 Fax: 919-681-7139 Fax: 217-333-8286 E-mail: [email protected] E-mail: [email protected] Bruce S. McEwen Keith L Parker Harold and Margaret Milliken Hatch Division of Endocrinology Laboratory of Neuroendocrinology Room J6.106 The Rockefeller University University of Texas Southwestern Medical 1230 York Avenue Center New York, NY 10021 5323 Harry Hines Boulevard Phone: 212-327-8624 Dallas, TX 75390-8857 Fax: 212-327-8634 Phone: 214-648-5027 E-mail: [email protected] Fax: 214-648-5044 E-mail: [email protected] CORRESPONDENCE INFORMATION vii JoAnne S Richards Phyllis M Wise Department of Molecular and Cellular Division of Biological Sciences Biology University of California-Davis Baylor College of Medicine One Shields Avenue One Baylor Plaza Davis, CA 95616-8536 Houston, TX 77030 Phone: 530-752-4460 Phone: 713-798-6238 Fax: 530-752-2604 Fax: 713-790-1275 E-mail: [email protected] E-mail: [email protected] Debra J Wolgemuth Evan R. Simpson Department of Genetics and Development Prince Henry’s Institute of Medical Research Columbia University College of Physicians Monash Medical Centre & Surgeons Level 4, Block E 630 West 168th Street 246 Clayton Road Black Building 1613 Clayton, Victoria 3168 Australia New York, NY 10032 Phone: 011-61-3-9594-4397 Phone: 212-305-7900 Fax: 011-61-3-9594-6376 Fax: 212-305-6084 E-mail: [email protected] E-mail: [email protected] Cheryl L Walker Li-yuan Yu-Lee Department of Carcinogenesis Department of Medicine University of Texas MD Anderson Cancer Section on Immunology, Allergy and Center Rheumatology Science Park-Research Division Baylor College of Medicine Park Road 1C 1 Baylor Plaza Smithville, TX 78957 Houston, TX 77030 Phone: 512-237-9550 Phone: 713-798-4770 Fax: 512-237-2475 Fax: 713-798-5780 E-mail: [email protected] E-mail: [email protected] Cellular and Molecular Pathways Regulating Mammalian Sex Determination CHRISTOPHER TILMANN AND BLANCHE CAPEL Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710 ABSTRACT In mammals, sex is determined by the presence or absence of a single gene on the Y chromosome, Sry. Sry, a member of the high mobility group family of transcription factors, is required to initiate male-specific pathways and repress female-specific pathways. Expression of Sry in the gonad, beginning at 10.5 days postcoitum, leads to the differentiation of the somatic supporting cell precursors as Sertoli cells. These cells direct the other cells of the gonad into their respective lineages. Currently, no direct targets of Sry are known. A number of cellular pathways initiated by Sry are required for testis development. These include the proliferation of pre-Sertoli cells and commitment to the Sertoli lineage, migration of cells from the adjacent mesonephros, and formation of a male-specific vasculature. Work is underway to identify genes controlling these processes. These genes will then be linked to Sry. I. Introduction Organisms that display sexually dimorphic phenotypes have evolved a variety of mechanisms for determining sex. In worms and flies, sex is determined by the ratio of X chromosomes to autosomes (Parkhurst and Meneely, 1994; Cline and Meyer, 1996). Reptiles and fish use hormones, temperature, or environmental cues to determine sex (Shapiro, 1990; Pieau et al., 2001). In mammals, sex is determined genetically by the presence or absence of a Y chromosome (Swain and Lovell-Badge, 1999; Capel, 2000). In 1947, Alfred Jost showed that removal of the gonads from fetal rabbits resulted in the development of female secondary sex characteristics, whether the animal was XX or XY.
Recommended publications
  • Spatially Heterogeneous Choroid Plexus Transcriptomes Encode Positional Identity and Contribute to Regional CSF Production
    The Journal of Neuroscience, March 25, 2015 • 35(12):4903–4916 • 4903 Development/Plasticity/Repair Spatially Heterogeneous Choroid Plexus Transcriptomes Encode Positional Identity and Contribute to Regional CSF Production Melody P. Lun,1,3 XMatthew B. Johnson,2 Kevin G. Broadbelt,1 Momoko Watanabe,4 Young-jin Kang,4 Kevin F. Chau,1 Mark W. Springel,1 Alexandra Malesz,1 Andre´ M.M. Sousa,5 XMihovil Pletikos,5 XTais Adelita,1,6 Monica L. Calicchio,1 Yong Zhang,7 Michael J. Holtzman,7 Hart G.W. Lidov,1 XNenad Sestan,5 Hanno Steen,1 XEdwin S. Monuki,4 and Maria K. Lehtinen1 1Department of Pathology, and 2Division of Genetics, Boston Children’s Hospital, Boston, Massachusetts 02115, 3Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, Massachusetts 02118, 4Department of Pathology and Laboratory Medicine, University of California Irvine School of Medicine, Irvine, California 92697, 5Department of Neurobiology and Kavli Institute for Neuroscience, Yale School of Medicine, New Haven, Connecticut 06510, 6Department of Biochemistry, Federal University of Sa˜o Paulo, Sa˜o Paulo 04039, Brazil, and 7Pulmonary and Critical Care Medicine, Department of Medicine, Washington University, St Louis, Missouri 63110 A sheet of choroid plexus epithelial cells extends into each cerebral ventricle and secretes signaling factors into the CSF. To evaluate whether differences in the CSF proteome across ventricles arise, in part, from regional differences in choroid plexus gene expression, we defined the transcriptome of lateral ventricle (telencephalic) versus fourth ventricle (hindbrain) choroid plexus. We find that positional identitiesofmouse,macaque,andhumanchoroidplexiderivefromgeneexpressiondomainsthatparalleltheiraxialtissuesoforigin.We thenshowthatmolecularheterogeneitybetweentelencephalicandhindbrainchoroidplexicontributestoregion-specific,age-dependent protein secretion in vitro.
    [Show full text]
  • Alpha Actinin 4: an Intergral Component of Transcriptional
    ALPHA ACTININ 4: AN INTERGRAL COMPONENT OF TRANSCRIPTIONAL PROGRAM REGULATED BY NUCLEAR HORMONE RECEPTORS By SIMRAN KHURANA Submitted in partial fulfillment of the requirements for the degree of doctor of philosophy Thesis Advisor: Dr. Hung-Ying Kao Department of Biochemistry CASE WESTERN RESERVE UNIVERSITY August, 2011 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of SIMRAN KHURANA ______________________________________________________ PhD candidate for the ________________________________degree *. Dr. David Samols (signed)_______________________________________________ (chair of the committee) Dr. Hung-Ying Kao ________________________________________________ Dr. Edward Stavnezer ________________________________________________ Dr. Leslie Bruggeman ________________________________________________ Dr. Colleen Croniger ________________________________________________ ________________________________________________ May 2011 (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. TABLE OF CONTENTS LIST OF TABLES vii LIST OF FIGURES viii ACKNOWLEDEMENTS xii LIST OF ABBREVIATIONS xiii ABSTRACT 1 CHAPTER 1: INTRODUCTION Family of Nuclear Receptors 3 Mechanism of transcriptional regulation by co-repressors and co-activators 8 Importance of LXXLL motif of co-activators in NR mediated transcription 12 Cyclic recruitment of co-regulators on the target promoters 15 Actin and actin related proteins (ABPs) in transcription
    [Show full text]
  • Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases
    Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Olivares, Ana Maria, Oscar Andrés Moreno-Ramos, and Neena B. Haider. 2015. “Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases.” Journal of Experimental Neuroscience 9 (Suppl 2): 93-121. doi:10.4137/JEN.S25480. http:// dx.doi.org/10.4137/JEN.S25480. Published Version doi:10.4137/JEN.S25480 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27320246 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Journal name: Journal of Experimental Neuroscience Journal type: Review Year: 2015 Volume: 9(S2) Role of Nuclear Receptors in Central Nervous System Running head verso: Olivares et al Development and Associated Diseases Running head recto: Nuclear receptors development and associated diseases Supplementary Issue: Molecular and Cellular Mechanisms of Neurodegeneration Ana Maria Olivares1, Oscar Andrés Moreno-Ramos2 and Neena B. Haider1 1Department of Ophthalmology, Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA, USA. 2Departamento de Ciencias Biológicas, Facultad de Ciencias, Universidad de los Andes, Bogotá, Colombia. ABSTRACT: The nuclear hormone receptor (NHR) superfamily is composed of a wide range of receptors involved in a myriad of important biological processes, including development, growth, metabolism, and maintenance.
    [Show full text]
  • Full-Text PDF (Final Published Version)
    Alexander, S. P. H., Cidlowski, J. A., Kelly, E., Marrion, N. V., Peters, J. A., Faccenda, E., Harding, S. D., Pawson, A. J., Sharman, J. L., Southan, C., Davies, J. A., & CGTP Collaborators (2017). THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Nuclear hormone receptors. British Journal of Pharmacology, 174, S208-S224. https://doi.org/10.1111/bph.13880 Publisher's PDF, also known as Version of record License (if available): CC BY Link to published version (if available): 10.1111/bph.13880 Link to publication record in Explore Bristol Research PDF-document This is the final published version of the article (version of record). It first appeared online via Wiley at https://doi.org/10.1111/bph.13880 . Please refer to any applicable terms of use of the publisher. University of Bristol - Explore Bristol Research General rights This document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/red/research-policy/pure/user-guides/ebr-terms/ S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2017/18: Nuclear hormone receptors. British Journal of Pharmacology (2017) 174, S208–S224 THE CONCISE GUIDE TO PHARMACOLOGY 2017/18: Nuclear hormone receptors Stephen PH Alexander1, John A Cidlowski2, Eamonn Kelly3, Neil V Marrion3, John A Peters4, Elena Faccenda5, Simon D Harding5,AdamJPawson5, Joanna L Sharman5, Christopher Southan5, Jamie A Davies5 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical
    [Show full text]
  • Emx2 Is Required for Growth of the Hippocampus but Not for Hippocampal Field Specification
    The Journal of Neuroscience, April 1, 2000, 20(7):2618–2625 Emx2 Is Required for Growth of the Hippocampus But Not for Hippocampal Field Specification Shubha Tole,1 Guy Goudreau,2 Stavroula Assimacopoulos,1 and Elizabeth A. Grove1 1Department of Neurobiology, Pharmacology, and Physiology, University of Chicago, Chicago, Illinois 60637, and 2Max Planck Institute of Biophysical Chemistry, D-37077 Goettingen, Germany The vertebrate Emx genes are expressed in a nested pattern in positioned in the Emx2 mutant. In particular, a dentate cell early embryonic cerebral cortex, such that a medial strip of population is generated, although it fails to form a morpholog- cortex expresses Emx2 but not Emx1. This pattern suggests ical gyrus. This failure may be part of a more widespread medial that Emx genes could play a role in specifying different areas or cortical defect in the mutant. Examination of cortical cell pro- fields of the cortex along the mediolateral axis. Such a role has liferation and differentiation indicates a disruption of the matu- been supported by the observation that in mice lacking func- ration of the medial cortex in the absence of Emx2. Thus, Emx2 tional Emx2 the hippocampus is shrunken and the most medial is required for normal growth and maturation of the hippocam- field of the cortex, the hippocampal dentate gyrus, appears by pus but not for the specification of cells to particular hippocam- cytoarchitecture to be missing (Pellegrini et al., 1996; Yoshida et pal field identities. al., 1997). Use of region-specific molecular markers shows, Key words: Emx2; hippocampus; patterning; specification; however, that hippocampal fields are specified and correctly cortical maturation; cortical hem The hippocampus, like the rest of the cerebral cortex, is divided Reports that specific mutations lead to morphological defects in into cytoarchitectonic areas or fields (Nauta and Feirtag, 1986).
    [Show full text]
  • Alternative Splicing in the Nuclear Receptor Superfamily Expands Gene Function to Refine Endo-Xenobiotic Metabolism S
    Supplemental material to this article can be found at: http://dmd.aspetjournals.org/content/suppl/2020/01/24/dmd.119.089102.DC1 1521-009X/48/4/272–287$35.00 https://doi.org/10.1124/dmd.119.089102 DRUG METABOLISM AND DISPOSITION Drug Metab Dispos 48:272–287, April 2020 Copyright ª 2020 by The American Society for Pharmacology and Experimental Therapeutics Minireview Alternative Splicing in the Nuclear Receptor Superfamily Expands Gene Function to Refine Endo-Xenobiotic Metabolism s Andrew J. Annalora, Craig B. Marcus, and Patrick L. Iversen Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, Oregon (A.J.A., C.B.M., P.L.I.) and United States Army Research Institute for Infectious Disease, Frederick, Maryland (P.L.I.) Received August 16, 2019; accepted December 31, 2019 ABSTRACT Downloaded from The human genome encodes 48 nuclear receptor (NR) genes, whose Exon inclusion options are differentially distributed across NR translated products transform chemical signals from endo- subfamilies, suggesting group-specific conservation of resilient func- xenobiotics into pleotropic RNA transcriptional profiles that refine tionalities. A deeper understanding of this transcriptional plasticity drug metabolism. This review describes the remarkable diversifica- expands our understanding of how chemical signals are refined and tion of the 48 human NR genes, which are potentially processed into mediated by NR genes. This expanded view of the NR transcriptome over 1000 distinct mRNA transcripts by alternative splicing (AS). The informs new models of chemical toxicity, disease diagnostics, and dmd.aspetjournals.org average human NR expresses ∼21 transcripts per gene and is precision-based approaches to personalized medicine.
    [Show full text]
  • The Role of Emx1 and Emx2 in the Developing Chick Telencephalon
    The Role of Emx1 and Emx2 in the developing chick telencephalon Dissertation Zur Erlangung des Doktorgrades der Naturwissenschaften (Dr.rer.nat.) der Fakultät für Biologie der Ludwig-Maximilian-Universität München Angefertigt am Max-Planck-Institut für Neurobiologie in der Arbeitsgruppe Neuronale Spezifizierung und in der GSF am Institut für Stammzellforschung Julia von Frowein München, Dezember 2004 1. Gutachter: Prof.Dr. Magdalena Götz 2. Gutachter: Prof.Dr. George Boyan eingereicht am 20.12.2004 Tag der mündlichen Prüfung: 26.4.2005 If the brain were so simple we could understand it, we would be so simple we couldn't. Lyall Watson Table of content 1 Table of content 1 Table of content...........................................................................................1 2 Abstract ........................................................................................................5 3 Zusammenfassung......................................................................................6 4 Introduction..................................................................................................8 4.1 General development of the regions of the central nervous system ....................................8 4.2 Patterning and regionalization .............................................................................................8 4.3 Regions of the forebrain.....................................................................................................10 4.4 Migration............................................................................................................................12
    [Show full text]
  • Figure S1. Basic Information of RNA-Seq Results. (A) Bar Plot of Reads Component for Each Sample
    Figure S1. Basic information of RNA-seq results. (A) Bar plot of reads component for each sample. (B) Dot plot shows the principal component analysis (PCA) of each sample. (C) Venn diagram of DEGs for three time points, the overlap part of the circles represents common differentially expressed genes between combinations. Figure S2. Scatter plot of DEGs for each time point. The X and Y axes represent the logarithmic value of gene expression. Red represents up-regulated DEG, blue represents down-regulated DEG, and gray represents non-DEG. Table S1. Primers used for quantitative real-time PCR analysis of DEGs. Gene Primer Sequence Forward 5’-CTACGAGTGGATGGTCAAGAGC-3’ FOXO1 Reverse 5’-CCAGTTCCTTCATTCTGCACACG-3’ Forward 5’-GACGTCCGGCATCAGAGAAA-3’ IRS2 Reverse 5’-TCCACGGCTAATCGTCACAG-3’ Forward 5’-CACAACCAGGACCTCACACC-3’ IRS1 Reverse 5’-CTTGGCACGATAGAGAGCGT-3’ Forward 5’-AGGATACCACTCCCAACAGACCT-3’ IL6 Reverse 5’-CAAGTGCATCATCGTTGTTCATAC-3’ Forward 5’-TCACGTTGTACGCAGCTACC-3’ CCL5 Reverse 5’-CAGTCCTCTTACAGCCTTTGG-3’ Forward 5’-CTGTGCAGCCGCAGTGCCTACC-3’ BMP7 Reverse 5’-ATCCCTCCCCACCCCACCATCT-3’ Forward 5’-CTCTCCCCCTCGACTTCTGA-3’ BCL2 Reverse 5’-AGTCACGCGGAACACTTGAT-3’ Forward 5’-CTGTCGAACACAGTGGTACCTG-3’ FGF7 Reverse 5’-CCAACTGCCACTGTCCTGATTTC-3’ Forward 5’-GGGAGCCAAAAGGGTCATCA-3’ GAPDH Reverse 5’-CGTGGACTGTGGTCATGAGT-3’ Supplementary material: Differentially expressed genes log2(SADS-CoV_12h/ Qvalue (SADS-CoV _12h/ Gene Symbol Control_12h) Control_12h) PTGER4 -1.03693 6.79E-04 TMEM72 -3.08132 3.66E-04 IFIT2 -1.02918 2.11E-07 FRAT2 -1.09282 4.66E-05
    [Show full text]
  • WO 2019/089982 Al 09 May 2019 (09.05.2019) W 1P O PCT
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2019/089982 Al 09 May 2019 (09.05.2019) W 1P O PCT (51) International Patent Classification: (71) Applicant: JUNO THERAPEUTICS, INC. [US/US]; 400 C12Q 1/6897 (2018.01) CI2N 15/65 (2006.01) Dexter Avenue N, Suite 1200, Seattle, Washington 98109 C12Q 1/02 (2006.01) G01N 33/50 (2006.01) (US). C12N 5/0783 (2010.01) (72) Inventors: AMIN, Rupesh; 400 Dexter Avenue N., Suite (21) International Application Number: 1200, Seattle, Washington 98109 (US). CHEN, Aye; 400 PCT/US20 18/058781 Dexter Avenue N., Suite 1200, Seattle, Washington 98109 (US). (22) International Filing Date: 0 1 November 2018 (01. 11.2018) (74) Agent: AHN, Sejin et al.; Morrison & Foerster LLP, 1253 1 High Bluff Drive, Suite 100, San Diego, California (25) Filing Language: English 92130-2040 (US). (26) Publication Language: English (81) Designated States (unless otherwise indicated, for every (30) Priority Data: kind of national protection available): AE, AG, AL, AM, 62/580,405 0 1 November 2017 (01. 11.2017) US AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, 62/596,758 08 December 2017 (08. 12.2017) US CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, 62/599,672 15 December 2017 (15. 12.2017) US DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, (54) Title: METHOD OF ASSESSING ACTIVITY OF RECOMBINANT ANTIGEN RECEPTORS FIG.
    [Show full text]
  • Conversion of Cerebral Cortex Into Basal Ganglia in Emx2 Pax6 Double
    articles Conversion of cerebral cortex into basal ganglia in Emx2 –/– Pax6Sey/Sey double-mutant mice Luca Muzio1, Barbara DiBenedetto1, Anastassia Stoykova2, Edoardo Boncinelli3, Peter Gruss2 and Antonello Mallamaci1 1 Department of Biological and Technological Research (DIBIT), Istituto Scientifico H. San Raffaele, via Olgettina 58, 20132 Milan, Italy 2 Max-Planck Institute of Biophysical Chemistry, Am Fassberg, 37018 Goettingen, Germany 3 International School for Advanced Studies, via Beirut 2/4, 34014 Trieste, Italy Correspondence should be addressed to A.M. ([email protected]) Published online: 15 July 2002, doi:10.1038/nn892 The molecular mechanisms that activate morphogenesis of cerebral cortex are currently the subject of intensive experimental analysis. Transcription factor genes of the homeobox, basic helix-loop- helix (bHLH) and zinc-finger families have recently been shown to have essential roles in this process. However, the actual selector genes activating corticogenesis have not yet been identified. Here we show that high-level expression of at least one functional allele of either of the homeobox genes Emx2 or Pax6 in the dorsal telencephalon is necessary and sufficient to stably activate morphogenesis of cerebral cortex and to repress that of adjacent structures, such as striatum. The molecular mechanisms that trigger morphogenesis of cere- morphologically and molecularly distinguishable from adjacent © http://neurosci.nature.com Group 2002 Nature Publishing bral cortex instead of adjacent telencephalic structures,
    [Show full text]
  • Effects of Maternal Undernutrition During Lactation on Aromatase, Estrogen, and Androgen Receptors Expression in Rat Testis at Weaning
    301 Effects of maternal undernutrition during lactation on aromatase, estrogen, and androgen receptors expression in rat testis at weaning Cı´ntia Vilanova Teixeira, Dorothe´e Silandre1, Alba Marcelly de Souza Santos, Christelle Delalande1, Francisco J B Sampaio, Serge Carreau1 and Cristiane da Fonte Ramos Urogenital Research Unit, State University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil 1Biochemistry, INRA2006-EA2608, University, Esplanade de la Paix, 14032, CAEN-Cedex, France (Requests for offprints should be addressed to S Carreau; Email: [email protected]) (C da Fonte Ramos is in US postdoctoral position at Stanford University, Department of Urology, California, USA). Abstract The goal of this study was to evaluate the effects of maternal concentration (ng/ml) was significantly higher in the PER malnutrition during lactation on serum levels of testosterone group compared with ER and C groups (CZ0.09G0.012; and estradiol, testicular testosterone concentration, aromatase, PERZ0.45G0.04; ERZ0.15G0.03, P!0.01). Testicular testicular androgen (AR) and estrogen a (ERa) receptors testosterone concentration (CZ2.1G0.43; PERZ6.5G0.7; expression in the pups at weaning. From parturition until ERZ13G2.3, P!0.01) was increased in treated groups weaning, Wistar rats were separated into three groups: (C) when compared with controls. The estradiol serum concen- control group, with free access to a standard laboratory diet tration (pg/ml) was lower in both dietary groups (CZ74G containing 23% protein; protein-energy restricted (PER) 4.6; PERZ49G3.2; ERZ60G5.5, P!0.01). The amounts group, with free access to an isoenergy and protein-restricted of aromatase mRNA and ERa transcripts were significantly diet containing 8% protein; and energy-restricted (ER) lower (P!0.05) in PER and ER groups; conversely AR (both group, receiving standard laboratory diet in restricted mRNA and protein) was significantly enhanced (P!0.05) in quantities, which were calculated according to the mean treated animals.
    [Show full text]
  • Rs 000-000-260 AKT/Pkba Substrate 1.0 Mg/Ml 500 Μ
    Catalog Number Display Name Concentration ValueSize Default Unit List price - Rs 000-000-260 AKT/PKBa Substrate 1.0 mg/mL 500 µg 24,434.00 000-000-264 NFKB p65 (Rel A) pS276 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-264NP NFKB p65 (Rel A) S276 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-266 p65 (Rel A) pS529 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-266NP p65 (Rel A) S529 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-383 DYKDDDDK (FLAG®) Peptide 1 mg/mL 1.0 mg 12,285.00 000-000-398 ATM S1981 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-400 ATM pS1981 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-401 AKT Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-402 Angiopoietin 2 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-403 Angiopoietin 1 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-404 Osteopontin Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-405 NOTCH 1 (intra) (Human specific) Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-407 NOTCH 1 (Human specific) Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-408 NOTCH 2 (Human specific) Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-410 ASK-1 phospho specific pS83 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-410NP ASK-1 non phospho specific S83 Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-433 Huntington pS421 Control Phospho Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-450 Huntington S421 Control Non-Phospho Peptide 1.0 mg/mL 50 µg 13,787.00 000-000-H47 Triple FLAG® Peptide 1.0 mg/ml 1.0 mg 12,285.00 000-000-K95 Beta Amyloid 40, Peptide 1.0 mg/mL 1.0 mg 1,06,334.00 000-000-K95S Beta Amyloid 40, Peptide 1.0 mg/mL 0.5 mg 27,164.00 000-000-M33 LL-37, Rhodamine
    [Show full text]