Numerical Index
Total Page：16
File Type：pdf, Size：1020Kb
Load more
Recommended publications
-
Cellular Responses to Erbb-2 Overexpression in Human Mammary Luminal Epithelial Cells: Comparison of Mrna and Protein Expression
British Journal of Cancer (2004) 90, 173 – 181 & 2004 Cancer Research UK All rights reserved 0007 – 0920/04 $25.00 www.bjcancer.com Cellular responses to ErbB-2 overexpression in human mammary luminal epithelial cells: comparison of mRNA and protein expression SL White1, S Gharbi1, MF Bertani1, H-L Chan1, MD Waterfield1 and JF Timms*,1 1 Ludwig Institute for Cancer Research, Wing 1.1, Cruciform Building, Gower Street, London WCIE 6BT, UK Microarray analysis offers a powerful tool for studying the mechanisms of cellular transformation, although the correlation between mRNA and protein expression is largely unknown. In this study, a microarray analysis was performed to compare transcription in response to overexpression of the ErbB-2 receptor tyrosine kinase in a model mammary luminal epithelial cell system, and in response to the ErbB-specific growth factor heregulin b1. We sought to validate mRNA changes by monitoring changes at the protein level using a parallel proteomics strategy, and report a surprisingly high correlation between transcription and translation for the subset of genes studied. We further characterised the identified targets and relate differential expression to changes in the biological properties of ErbB-2-overexpressing cells. We found differential regulation of several key cell cycle modulators, including cyclin D2, and downregulation of a large number of interferon-inducible genes, consistent with increased proliferation of the ErbB-2- overexpressing cells. Furthermore, differential expression of genes involved in extracellular matrix modelling and cellular adhesion was linked to altered adhesion of these cells. Finally, we provide evidence for enhanced autocrine activation of MAPK signalling and the AP-1 transcription complex. -
Neuromedin U Directly Stimulates Growth of Cultured Rat Calvarial Osteoblast-Like Cells Acting Via the NMU Receptor 2 Isoform
363-368 1/8/08 15:53 Page 363 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 22: 363-368, 2008 363 Neuromedin U directly stimulates growth of cultured rat calvarial osteoblast-like cells acting via the NMU receptor 2 isoform MARCIN RUCINSKI, AGNIESZKA ZIOLKOWSKA, MARIANNA TYCZEWSKA, MARTA SZYSZKA and LUDWIK K. MALENDOWICZ Department of Histology and Embryology, Poznan University of Medical Sciences, 6 Swiecicki St., 60-781 Poznan, Poland Received April 4, 2008; Accepted June 2, 2008 DOI: 10.3892/ijmm_00000031 Abstract. The neuromedin U (NMU) system is composed of nervous system. Among others, peptides involved in regulation NMU, neuromedin S (NMS) and their receptors NMUR1 and of energy homeostasis belong to this group of compounds NMUR2. This system is involved in the regulation of energy (1-3), and the best recognised is leptin, an adipocyte-derived homeostasis, neuroendocrine functions, immune response, anorexigenic hormone, which plays a role in regulating bone circadian rhythm and spermatogenesis. The present study formation. Acting directly this pleiotropic cytokine exerts a aimed to investigate the possible role of the NMU system in stimulatory effect on bone formation. While acting through regulating functions of cultured rat calvarial osteoblast-like the central nervous system (CNS) leptin suppresses bone (ROB) cells. By using QPCR, high expression of NMU formation (4-10). Moreover, OB-Rb mRNA is expressed in mRNA was found in freshly isolated ROB cells while after 7, osteoblasts, and in vitro leptin enhances their proliferation 14, and 21 days of culture, expression of the studied gene and has no effect on osteocalcin and osteopontin production by was very low. -
CURRICULUM VITAE Joseph S. Takahashi Howard Hughes Medical
CURRICULUM VITAE Joseph S. Takahashi Howard Hughes Medical Institute Department of Neuroscience University of Texas Southwestern Medical Center 5323 Harry Hines Blvd., NA4.118 Dallas, Texas 75390-9111 (214) 648-1876, FAX (214) 648-1801 Email: [email protected] DATE OF BIRTH: December 16, 1951 NATIONALITY: U.S. Citizen by birth EDUCATION: 1981-1983 Pharmacology Research Associate Training Program, National Institute of General Medical Sciences, Laboratory of Clinical Sciences and Laboratory of Cell Biology, National Institutes of Health, Bethesda, MD 1979-1981 Ph.D., Institute of Neuroscience, Department of Biology, University of Oregon, Eugene, Oregon, Dr. Michael Menaker, Advisor. Summer 1977 Hopkins Marine Station, Stanford University, Pacific Grove, California 1975-1979 Department of Zoology, University of Texas, Austin, Texas 1970-1974 B.A. in Biology, Swarthmore College, Swarthmore, Pennsylvania PROFESSIONAL EXPERIENCE: 2013-present Principal Investigator, Satellite, International Institute for Integrative Sleep Medicine, World Premier International Research Center Initiative, University of Tsukuba, Japan 2009-present Professor and Chair, Department of Neuroscience, UT Southwestern Medical Center 2009-present Loyd B. Sands Distinguished Chair in Neuroscience, UT Southwestern 2009-present Investigator, Howard Hughes Medical Institute, UT Southwestern 2009-present Professor Emeritus of Neurobiology and Physiology, and Walter and Mary Elizabeth Glass Professor Emeritus in the Life Sciences, Northwestern University -
Endothelin-2 Signaling in the Neural Retina Promotes the Endothelial Tip Cell State and Inhibits Angiogenesis
Endothelin-2 signaling in the neural retina promotes PNAS PLUS the endothelial tip cell state and inhibits angiogenesis Amir Rattnera,1, Huimin Yua, John Williamsa,b, Philip M. Smallwooda,b, and Jeremy Nathansa,b,c,d,1 Departments of aMolecular Biology and Genetics, cNeuroscience, and dOphthalmology and bHoward Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21205 Contributed by Jeremy Nathans, August 20, 2013 (sent for review February 19, 2013) Endothelin signaling is required for neural crest migration and time lapse imaging studies of vascular development in zebrafish homeostatic regulation of blood pressure. Here, we report that and mammalian EC dynamics in explant culture show that the tip constitutive overexpression of Endothelin-2 (Edn2) in the mouse cell and stalk cell states are highly plastic, with frequent retina perturbs vascular development by inhibiting endothelial cell exchanges between the two cell states (8, 9). migration across the retinal surface and subsequent endothelial Several other signaling pathways are also essential for retinal cell invasion into the retina. Developing endothelial cells exist in vascular development. Norrin, a Muller-glia–derived ligand, and one of two states: tip cells at the growing front and stalk cells in its EC receptor Frizzled4 (Fz4), coreceptor Lrp5, and receptor the vascular plexus behind the front. This division of endothelial chaperone Tspan12 activate canonical Wnt signaling in de- cell states is one of the central organizing principles of angiogen- veloping ECs (10). In humans and mice, defects in any of these esis. In the developing retina, Edn2 overexpression leads to components lead to retinal hypovascularization. -
ADIPOR1 Is Essential for Vision and Its RPE Expression Is Lost in the Mfrp Valentin M Sluch
The Jackson Laboratory The Mouseion at the JAXlibrary Faculty Research 2018 Faculty Research 9-25-2018 ADIPOR1 is essential for vision and its RPE expression is lost in the Mfrp Valentin M Sluch Angela Banks Hui Li Maura A Crowley Vanessa Davis See next page for additional authors Follow this and additional works at: https://mouseion.jax.org/stfb2018 Part of the Life Sciences Commons, and the Medicine and Health Sciences Commons Recommended Citation Sluch, Valentin M; Banks, Angela; Li, Hui; Crowley, Maura A; Davis, Vanessa; Xiang, Chuanxi; Yang, Junzheng; Demirs, John T; Vrouvlianis, Joanna; Leehy, Barrett; Hanks, Shawn; Hyman, Alexandra M; Aranda, Jorge; Chang, Bo; Bigelow, Chad E; and Rice, Dennis S, "ADIPOR1 is essential for vision and its RPE expression is lost in the Mfrp" (2018). Faculty Research 2018. 197. https://mouseion.jax.org/stfb2018/197 This Article is brought to you for free and open access by the Faculty Research at The ousM eion at the JAXlibrary. It has been accepted for inclusion in Faculty Research 2018 by an authorized administrator of The ousM eion at the JAXlibrary. For more information, please contact [email protected]. Authors Valentin M Sluch, Angela Banks, Hui Li, Maura A Crowley, Vanessa Davis, Chuanxi Xiang, Junzheng Yang, John T Demirs, Joanna Vrouvlianis, Barrett Leehy, Shawn Hanks, Alexandra M Hyman, Jorge Aranda, Bo Chang, Chad E Bigelow, and Dennis S Rice This article is available at The ousM eion at the JAXlibrary: https://mouseion.jax.org/stfb2018/197 www.nature.com/scientificreports OPEN ADIPOR1 is essential for vision and its RPE expression is lost in the Mfrprd6 mouse Received: 20 April 2018 Valentin M. -
Different Distribution of Neuromedin S and Its Mrna in the Rat Brain: NMS Peptide Is Present Not Only in the Hypothalamus As the Mrna, but Also in the Brainstem
ORIGINAL RESEARCH ARTICLE published: 03 December 2012 doi: 10.3389/fendo.2012.00152 Different distribution of neuromedin S and its mRNA in the rat brain: NMS peptide is present not only in the hypothalamus as the mRNA, but also in the brainstem Miwa Mori 1†, Kenji Mori 1†,Takanori Ida2,Takahiro Sato3, Masayasu Kojima3, Mikiya Miyazato1* and Kenji Kangawa1 1 Department of Biochemistry, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan 2 Interdisciplinary Research Organization, University of Miyazaki, Miyazaki, Japan 3 Molecular Genetics, Institute of Life Sciences, Kurume University, Fukuoka, Japan Edited by: Neuromedin S (NMS) is a neuropeptide identified as another endogenous ligand for two Hubert Vaudry, University of Rouen, orphan G protein-coupled receptors, FM-3/GPR66 and FM-4/TGR-1, which have also been France identified as types 1 and 2 receptors for neuromedin U structurally related to NMS. Although Reviewed by: expression of NMS mRNA is found mainly in the brain, spleen, and testis, the distribution of Etienne Challet, Centre National de la Recherche Scientifique, France its peptide has not yet been investigated. Using a newly prepared antiserum, we developed Manuel Tena-Sempere, University of a highly sensitive radioimmunoassay for rat NMS. NMS peptide was clearly detected in the Cordoba, Spain rat brain at a concentration of 68.3 ± 3.4 fmol/g wet weight, but it was hardly detected in the *Correspondence: spleen and testis. A high content of NMS peptide was found in the hypothalamus, midbrain, Mikiya Miyazato, Department of and pons–medulla oblongata, whereas abundant expression of NMS mRNA was detected Biochemistry, National Cerebral and Cardiovascular Center Research only in the hypothalamus. -
A 0.70% E 0.80% Is 0.90%
US 20080317666A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2008/0317666 A1 Fattal et al. (43) Pub. Date: Dec. 25, 2008 (54) COLONIC DELIVERY OF ACTIVE AGENTS Publication Classification (51) Int. Cl. (76) Inventors: Elias Fattal, Paris (FR); Antoine A6IR 9/00 (2006.01) Andremont, Malakoff (FR); A61R 49/00 (2006.01) Patrick Couvreur, A6II 5L/12 (2006.01) Villebon-sur-Yvette (FR); Sandrine A6IPI/00 (2006.01) Bourgeois, Lyon (FR) (52) U.S. Cl. .......................... 424/1.11; 424/423; 424/9.1 (57) ABSTRACT Correspondence Address: Drug delivery devices that are orally administered, and that David S. Bradlin release active ingredients in the colon, are disclosed. In one Womble Carlyle Sandridge & Rice embodiment, the active ingredients are those that inactivate P.O.BOX 7037 antibiotics, such as macrollides, quinolones and beta-lactam Atlanta, GA 30359-0037 (US) containing antibiotics. One example of a Suitable active agent is an enzyme Such as beta-lactamases. In another embodi ment, the active agents are those that specifically treat colonic (21) Appl. No.: 11/628,832 disorders, such as Chrohn's Disease, irritable bowel syn drome, ulcerative colitis, colorectal cancer or constipation. (22) PCT Filed: Feb. 9, 2006 The drug delivery devices are in the form of beads of pectin, crosslinked with calcium and reticulated with polyethylene imine. The high crosslink density of the polyethyleneimine is (86). PCT No.: PCT/GBO6/OO448 believed to stabilize the pectin beads for a sufficient amount of time such that a Substantial amount of the active ingredi S371 (c)(1), ents can be administered directly to the colon. -
Mechanisms of Skeletal Disease Mediated by Haematological
OF z a ) n Mechanisms of Skeletal Disease Mediated by Haematolo gical Malignancies Beiqing Pan B. Med. M. Med. Sc. Matthew Roberts Laboratory, Hanson Institute, Institute of Medical and Veterinary Science Department of Medicine, The University of Adelaide, South Australia A thesis submitted to the University of Adelaide in candidature for the degree of Doctor of Philosophy August 2004 TABLE OF CONTENTS DEGLARAT|ON......... """' l AGKNOWLEDGMENT.............. """' ll A8STRACT............. """'lv ABBREVIATIONS """""v1 PUBLICATIONS """"""'xl CHAPTER 1 GENERAL INTRODUCTION ......1 TO BONE 1.1 HAEMATOLOGICAL MALIGNANCIES WHICII GIBE RISE 1 LESIONS 2 1.1.1 Osteolytic Bone Disease Mediated by Multiple Myeloma 2 1.1.1.1 General Description...'.. 4 t.l.l.2 P athophysiolo gy of tvttvt 5 1.1.1.3 Osteolytic Bone Disease Lt.2 Osteoblastic Bone Disease Mediated by POEMS" 6 t.l.2.1 General DescriPtion...... 6 l.l.2.2 Pathophysiology of POEMS Syndrome. 1 8 1.1.2.3 Osteoblastic Bone Disease 1.2 BONE PHYSIOLOGY.............. 8 1.2.1 PhysiologicalBoneRemodelling 9 1.2.2 Bone ResorPtion 9 1.2.2.1 Osteoclasts 9 1.2.2.2 Osteoclast Stem Cells 1.2.3 BoneFormation.......'......... 1.2.3.1 Osteoblast Cells 1.2.3.2 OsteoblastStemCells..... 1.2.3.3 OsteocYtes '.".....' 1.2.3.4 Lining Cells FACTORS INVOLVED IN BONE LESIONS... t4 1.3 l6 1.3.1 Osteoclast Activating Factors (OAFÐ """"' 1.3.1.1 Interleukin-1P 16 1.3.1.2 Interleukin-6 t7 l8 1 .3.1 .3 Tumour Necrosis Factor-cx'...... 1.3.1.4 ParathyroidHormone Related Protein""""""' t9 1.3.2 RANKL/RANIIOPGSYStem 20 1.3.2.1 GeneralDescriPtion 20 1.3.2.2 RANKL/OPG Ratio and Bone Lesion 22 1.3.2.3 Incrçased RANKL/OPG Ratio in MM"' 22 1.3.2.4 The Regulation of RANKL/OPG Ratio in MM 23 1.3.3 Endothelin-1 (ET-l)'..'.'... -
Neuropeptides Controlling Energy Balance: Orexins and Neuromedins
Neuropeptides Controlling Energy Balance: Orexins and Neuromedins Joshua P. Nixon, Catherine M. Kotz, Colleen M. Novak, Charles J. Billington, and Jennifer A. Teske Contents 1 Brain Orexins and Energy Balance ....................................................... 79 1.1 Orexin............................................................................... 79 2 Orexin and Feeding ....................................................................... 80 3 Orexin and Arousal ....................................................................... 83 J.P. Nixon • J.A. Teske Veterans Affairs Medical Center, Research Service (151), Minneapolis, MN, USA Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA Minnesota Obesity Center, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA C.M. Kotz (*) Veterans Affairs Medical Center, GRECC (11 G), Minneapolis, MN, USA Veterans Affairs Medical Center, Research Service (151), Minneapolis, MN, USA Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA Minnesota Obesity Center, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA e-mail: [email protected] C.M. Novak Department of Biological Sciences, Kent State University, Kent, OH, USA C.J. Billington Veterans Affairs Medical Center, Research Service (151), Minneapolis, MN, USA Veterans Affairs Medical Center, Endocrine Unit (111 G), Minneapolis, MN, USA Department of Food Science and Nutrition, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA Minnesota Obesity Center, University of Minnesota, 1334 Eckles Avenue, St. Paul, MN 55108, USA H.-G. Joost (ed.), Appetite Control, Handbook of Experimental Pharmacology 209, 77 DOI 10.1007/978-3-642-24716-3_4, # Springer-Verlag Berlin Heidelberg 2012 78 J.P. Nixon et al. 4 Orexin Actions on Endocrine and Autonomic Systems ................................. 84 5 Orexin, Physical Activity, and Energy Expenditure .................................... -
Neuromedins U and S Involvement in the Regulation of the Hypothalamo–Pituitary–Adrenal Axis
REVIEW ARTICLE published: 05 December 2012 doi: 10.3389/fendo.2012.00156 Neuromedins U and S involvement in the regulation of the hypothalamo–pituitary–adrenal axis Ludwik K. Malendowicz*, Agnieszka Ziolkowska and Marcin Rucinski Department of Histology and Embryology, Poznan University of Medical Sciences, Poznan, Poland Edited by: We reviewed neuromedin U (NMU) and neuromedin S (NMS) involvement in the regulation Hubert Vaudry, University of Rouen, of the hypothalamo–pituitary–adrenal (HPA) axis function. NMU and NMS are structurally France related and highly conserved neuropeptides. They exert biological effects via two GPCR Reviewed by: receptors designated as NMUR1 and NMUR2 which show differential expression. NMUR1 James A. Carr, Texas Tech University, USA is expressed predominantly at the periphery, while NMUR2 in the central nervous system. Gábor B. Makara, Hungarian Elements of the NMU/NMS and their receptors network are also expressed in the HPA Academy of Sciences, Hungary axis and progress in molecular biology techniques provided new information on their *Correspondence: actions within this system. Several lines of evidence suggest that within the HPA axis Ludwik K. Malendowicz, NMU and NMS act at both hypothalamic and adrenal levels. Moreover, new data suggest Department of Histology and Embryology, Poznan University of that NMU and NMS are involved in central and peripheral control of the stress response. Medical Sciences, 6 Swie¸cickiSt., 60-781 Poznan, Poland. Keywords: neuromedin U, neuromedin S, hypothalamus, pituitary, adrenal e-mail: [email protected] INTRODUCTION Identification of specific NMU receptors (NMUR1 and In search for new biologically active peptides, the group of NMUR2) and its anorexigenic action have enhanced interest in Minamino, Kangawa, and Matsuo in the 1980s isolated numerous physiological role of NMU and NMS (Howard et al., 2000; Ida small neuropeptides from porcine spinal cord. -
Roles of Neuropeptides, VIP and AVP, in the Mammalian Central Circadian Clock
fnins-15-650154 April 11, 2021 Time: 10:52 # 1 MINI REVIEW published: 15 April 2021 doi: 10.3389/fnins.2021.650154 Roles of Neuropeptides, VIP and AVP, in the Mammalian Central Circadian Clock Daisuke Ono1,2*, Ken-ichi Honma3 and Sato Honma3* 1 Department of Neuroscience II, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan, 2 Department of Neural Regulation, Nagoya University Graduate School of Medicine, Nagoya, Japan, 3 Research and Education Center for Brain Science, Hokkaido University Graduate School of Medicine, Sapporo, Japan In mammals, the central circadian clock is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Individual SCN cells exhibit intrinsic oscillations, and their circadian period and robustness are different cell by cell in the absence of cellular coupling, indicating that cellular coupling is important for coherent circadian rhythms in the SCN. Several neuropeptides such as arginine vasopressin (AVP) and vasoactive intestinal polypeptide (VIP) are expressed in the SCN, where these neuropeptides function as synchronizers and are important for entrainment to environmental light and for determining the circadian period. These neuropeptides are also related to Edited by: developmental changes of the circadian system of the SCN. Transcription factors are Masayuki Ikeda, required for the formation of neuropeptide-related neuronal networks. Although VIP University of Toyama, Japan is critical for synchrony of circadian rhythms in the neonatal SCN, it is not required Reviewed by: Elizabeth S. Maywood, for synchrony in the embryonic SCN. During postnatal development, the clock genes MRC Laboratory of Molecular Biology cryptochrome (Cry)1 and Cry2 are involved in the maturation of cellular networks, and (LMB), United Kingdom William David Todd, AVP is involved in SCN networks. -
Endothelin-2 Deficiency Causes Growth Retardation, Hypothermia, and Emphysema in Mice
Endothelin-2 deficiency causes growth retardation, hypothermia, and emphysema in mice Inik Chang, … , Roderick R. McInnes, Masashi Yanagisawa J Clin Invest. 2013;123(6):2643-2653. https://doi.org/10.1172/JCI66735. Research Article Endocrinology To explore the physiological functions of endothelin-2 (ET-2), we generated gene-targeted mouse models. GlobalE t2 knockout mice exhibited severe growth retardation and juvenile lethality. Despite normal milk intake, they suffered from internal starvation characterized by hypoglycemia, ketonemia, and increased levels of starvation-induced genes. Although ET-2 is abundantly expressed in the gastrointestinal tract, the intestine was morphologically and functionally normal. Moreover, intestinal epithelium–specific Et2 knockout mice showed no abnormalities in growth and survival. Global Et2 knockout mice were also profoundly hypothermic. Housing Et2 knockout mice in a warm environment significantly extended their median lifespan. However, neuron-specific Et2 knockout mice displayed a normal core body temperature. Low levels of Et2 mRNA were also detected in the lung, with transient increases soon after birth. The lungs ofE t2 knockout mice showed emphysematous structural changes with an increase in total lung capacity, resulting in chronic hypoxemia, hypercapnia, and increased erythropoietin synthesis. Finally, systemically inducible ET-2 deficiency in neonatal and adult mice fully reproduced the phenotype previously observed in global Et2 knockout mice. Together, these findings reveal that ET-2 is critical for the growth and survival of postnatal mice and plays important roles in energy homeostasis, thermoregulation, and the maintenance of lung morphology and function. Find the latest version: https://jci.me/66735/pdf Research article Endothelin-2 deficiency causes growth retardation, hypothermia, and emphysema in mice Inik Chang,1 Alexa N.