Roles for -Synuclein in Gene Expression
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The Dopamine Transporter: More Exciting Than Housekeeping
The Dopamine Transporter: More Exciting than Housekeeping Susan Ingram Washington State University Vancouver Dopaminergic Synapse Presynaptic cell MGluR 2 Na+ Cl- GIRK D2 DA DA D2 D1 a1 Postsynaptic cell Currents are activated at lower dopamine concentrations than are required for transport Ingram, et al., 2002 Low DA concentrations increase firing Ingram, et al., 2002 DAT-mediated chloride current is excitatory in cultured midbrain DA neurons DEPOLARIZATION HYPERPOLARIZATION Ingram, et al., 2002 Proteins that regulate intracellular Cl- Whole-cell patch clamp recordings from DA neurons Raclopride Sulpiride Prazosin TTX biocytin Prasad and Amara, 2001 Amphetamine activates a DAT-mediated current at low concentrations Cultures Slices Watts, Fyfe and Ingram, unpublished data. DA neurons make glutamatergic autapses in culture and amphetamine increases AMPA currents Ingram, et al., unpublished data mbYFPQS localizes to the membrane of cultured midbrain neurons Watts, Jimenez and Ingram, unpublished data. Amphetamine stimulates a dose-dependent change in mbYFPQS fluorescence in both soma and dendrites of DA neurons Watts and Ingram, unpublished data. KCC2 Expression is different in cultures and slices cultures slices TH KCC2 Jamieson and Ingram, unpublished data. Baculoviral Transfections Watts and Ingram, unpublished data. Summary • DAT-mediated chloride current may alter excitability of DA neurons and integration of synaptic activity. • The current may be activated selectively (relative to transport) by low DA and amphetamine concentrations suggesting a role in increasing release of DA. • The amphetamine-mediated current is dose-dependent in both cultures and slices of midbrain neurons but is inhibited at high amphetamine concentrations (20 µM). • The mbYFPQS is a sensitive tool to measure intracellular chloride concentrations (K50 = 30 mM) and is useful for monitoring changes in intracellular chloride concentrations in dendrites. -
CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells
CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells Shweta Jain, Sathi Babu Chodisetti, Javed N. Agrewala* Immunology Laboratory, Institute of Microbial Technology, Council of Scientific and Industrial Research, Chandigarh, India Abstract Conventionally, signaling through BCR initiates sequence of events necessary for activation and differentiation of B cells. We report an alternative approach, independent of BCR, for stimulating resting B (RB) cells, by involving TLR-2 and CD40 - molecules crucial for innate and adaptive immunity. CD40 triggering of TLR-2 stimulated RB cells significantly augments their activation, proliferation and differentiation. It also substantially ameliorates the calcium flux, antigen uptake capacity and ability of B cells to activate T cells. The survival of RB cells was improved and it increases the number of cells expressing activation induced deaminase (AID), signifying class switch recombination (CSR). Further, we also observed increased activation rate and decreased threshold period required for optimum stimulation of RB cells. These results corroborate well with microarray gene expression data. This study provides novel insights into coordination between the molecules of innate and adaptive immunity in activating B cells, in a BCR independent manner. This strategy can be exploited to design vaccines to bolster B cell activation and antigen presenting efficiency, leading to faster and better immune response. Citation: Jain S, Chodisetti SB, Agrewala JN (2011) CD40 Signaling Synergizes with TLR-2 in the BCR Independent Activation of Resting B Cells. PLoS ONE 6(6): e20651. doi:10.1371/journal.pone.0020651 Editor: Leonardo A. Sechi, Universita di Sassari, Italy Received April 14, 2011; Accepted May 6, 2011; Published June 2, 2011 Copyright: ß 2011 Jain et al. -
An Overview of the Role of Hdacs in Cancer Immunotherapy
International Journal of Molecular Sciences Review Immunoepigenetics Combination Therapies: An Overview of the Role of HDACs in Cancer Immunotherapy Debarati Banik, Sara Moufarrij and Alejandro Villagra * Department of Biochemistry and Molecular Medicine, School of Medicine and Health Sciences, The George Washington University, 800 22nd St NW, Suite 8880, Washington, DC 20052, USA; [email protected] (D.B.); [email protected] (S.M.) * Correspondence: [email protected]; Tel.: +(202)-994-9547 Received: 22 March 2019; Accepted: 28 April 2019; Published: 7 May 2019 Abstract: Long-standing efforts to identify the multifaceted roles of histone deacetylase inhibitors (HDACis) have positioned these agents as promising drug candidates in combatting cancer, autoimmune, neurodegenerative, and infectious diseases. The same has also encouraged the evaluation of multiple HDACi candidates in preclinical studies in cancer and other diseases as well as the FDA-approval towards clinical use for specific agents. In this review, we have discussed how the efficacy of immunotherapy can be leveraged by combining it with HDACis. We have also included a brief overview of the classification of HDACis as well as their various roles in physiological and pathophysiological scenarios to target key cellular processes promoting the initiation, establishment, and progression of cancer. Given the critical role of the tumor microenvironment (TME) towards the outcome of anticancer therapies, we have also discussed the effect of HDACis on different components of the TME. We then have gradually progressed into examples of specific pan-HDACis, class I HDACi, and selective HDACis that either have been incorporated into clinical trials or show promising preclinical effects for future consideration. -
The Roles of Histone Deacetylase 5 and the Histone Methyltransferase Adaptor WDR5 in Myc Oncogenesis
The Roles of Histone Deacetylase 5 and the Histone Methyltransferase Adaptor WDR5 in Myc oncogenesis By Yuting Sun This thesis is submitted in fulfilment of the requirements for the degree of Doctor of Philosophy at the University of New South Wales Children’s Cancer Institute Australia for Medical Research School of Women’s and Children’s Health, Faculty of Medicine University of New South Wales Australia August 2014 PLEASE TYPE THE UNIVERSITY OF NEW SOUTH WALES Thesis/Dissertation Sheet Surname or Family name: Sun First name: Yuting Other name/s: Abbreviation for degree as given in the University calendar: PhD School : School of·Women's and Children's Health Faculty: Faculty of Medicine Title: The Roles of Histone Deacetylase 5 and the Histone Methyltransferase Adaptor WDR5 in Myc oncogenesis. Abstract 350 words maximum: (PLEASE TYPE) N-Myc Induces neuroblastoma by regulating the expression of target genes and proteins, and N-Myc protein is degraded by Fbxw7 and NEDD4 and stabilized by Aurora A. The class lla histone deacetylase HDAC5 suppresses gene transcription, and blocks myoblast and leukaemia cell differentiation. While histone H3 lysine 4 (H3K4) trimethylation at target gene promoters is a pre-requisite for Myc· induced transcriptional activation, WDRS, as a histone H3K4 methyltransferase presenter, is required for H3K4 methylation and transcriptional activation mediated by a histone H3K4 methyltransferase complex. Here, I investigated the roles of HDAC5 and WDR5 in N-Myc overexpressing neuroblastoma. I have found that N-Myc upregulates HDAC5 protein expression, and that HDAC5 represses NEDD4 gene expression, increases Aurora A gene expression and consequently upregulates N-Myc protein expression in neuroblastoma cells. -
Program Book
PARKINSON’SDISEASE2014 ADVANCING RESEARCH, IMPROVING LIVES PROGRAM MATERIALS Sponsored by: January 6 – 7, 2014 Natcher Conference Center National Institutes of Health Bethesda, MD About our cover: The program cover image is a stylized version of the Parkinson’s Disease Motor-Related Pattern (PDRP), an abnormal pattern of regional brain function observed in MRI studies which shows increased metabolism indicated by red in some brain regions (pallidothalamic, pontine, and motor cortical areas), and decreased metabolism indicated by blue in others (associated lateral premotor and posterior parietal areas). Original image used with permission of David Eidelberg, M.D. For further information see: Hirano et al., Journal of Neuroscience 28 (16): 4201-4209. Welcome Message from Dr. Story C. Landis Welcome to the National Institute of Neurological Disorders and Stroke (NINDS) conference, “Parkinson’s Disease 2014: Advancing Research, Improving Lives.” Remarkable new discoveries and technological advances are rapidly changing the way we study the biological mechanisms of Parkinson’s disease, identify paths to improved treatments, and design effective clinical trials. Elucidating mechanisms and developing and testing effective interventions require a diverse set of approaches and perspectives. The NINDS has organized this conference with the primary goal of seeking consensus on, and prioritizing, research recommendations spanning clinical, translational, and basic Parkinson’s disease research that we support. We have assembled a stellar and dedicated group of session chairs and panelists who have worked collaboratively to identify emerging research opportunities in Parkinson’s research. While we have divided our working groups into three main research areas, we expect each will inform the others over the course of the next two days, and we look forward to both complementary and unique perspectives. -
Determining HDAC8 Substrate Specificity by Noah Ariel Wolfson A
Determining HDAC8 substrate specificity by Noah Ariel Wolfson A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy (Biological Chemistry) in the University of Michigan 2014 Doctoral Committee: Professor Carol A. Fierke, Chair Professor Robert S. Fuller Professor Anna K. Mapp Associate Professor Patrick J. O’Brien Associate Professor Raymond C. Trievel Dedication My thesis is dedicated to all my family, mentors, and friends who made getting to this point possible. ii Table of Contents Dedication ....................................................................................................................................... ii List of Figures .............................................................................................................................. viii List of Tables .................................................................................................................................. x List of Appendices ......................................................................................................................... xi Abstract ......................................................................................................................................... xii Chapter 1 HDAC8 substrates: Histones and beyond ...................................................................... 1 Overview ..................................................................................................................................... 1 HDAC introduction -
The Metabolic Regulator Histone Deacetylase 9 Contributes to Glucose Homeostasis
Page 1 of 53 Diabetes The metabolic regulator histone deacetylase 9 contributes to glucose homeostasis abnormality induced by hepatitis C virus infection Jizheng CHEN2, Ning WANG1, Mei DONG1, Min GUO2, Yang ZHAO3, Zhiyong ZHUO3, Chao ZHANG3, Xiumei CHI4, Yu PAN4, Jing JIANG4, Hong TANG2, Junqi NIU4, Dongliang YANG5, Zhong LI1, Xiao HAN1, Qian WANG1* and Xinwen Chen2 1 Jiangsu Province Key Lab of Human Functional Genomics, Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, 210029, China 2 State Key Lab of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China 3 Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China 4 Department of Hepatology, The First Hospital of Jilin University, Changchun, 130021, China 5 Department of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430074, China 1 Diabetes Publish Ahead of Print, published online September 29, 2015 Diabetes Page 2 of 53 *Correspondence: Qian WANG, Ph.D. Jiangsu Province Key Lab of Human Functional Genomics Department of Biochemistry and Molecular Biology Nanjing Medical University Nanjing 210029, China E-mail: [email protected] Fax: +86-25-8362 1065 Tel: +86-25-8686 2729 2 Page 3 of 53 Diabetes ABSTRACT Class IIa histone deacetylases (HDACs), such as HDAC4, HDAC5, and HDAC7 provide critical mechanisms for regulating glucose homeostasis. Here we report HDAC9, another class IIa HDAC, regulates hepatic gluconeogenesis via deacetylation of a Forkhead box O (FoxO) family transcription factor, FoxO1, together with HDAC3. Specifically, HDAC9 expression can be strongly induced upon hepatitis C virus (HCV) infection. -
Antigen-Specific Memory CD4 T Cells Coordinated Changes in DNA
Downloaded from http://www.jimmunol.org/ by guest on September 24, 2021 is online at: average * The Journal of Immunology The Journal of Immunology published online 18 March 2013 from submission to initial decision 4 weeks from acceptance to publication http://www.jimmunol.org/content/early/2013/03/17/jimmun ol.1202267 Coordinated Changes in DNA Methylation in Antigen-Specific Memory CD4 T Cells Shin-ichi Hashimoto, Katsumi Ogoshi, Atsushi Sasaki, Jun Abe, Wei Qu, Yoichiro Nakatani, Budrul Ahsan, Kenshiro Oshima, Francis H. W. Shand, Akio Ametani, Yutaka Suzuki, Shuichi Kaneko, Takashi Wada, Masahira Hattori, Sumio Sugano, Shinichi Morishita and Kouji Matsushima J Immunol Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Author Choice option Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Freely available online through http://www.jimmunol.org/content/suppl/2013/03/18/jimmunol.120226 7.DC1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material Permissions Email Alerts Subscription Author Choice Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 24, 2021. Published March 18, 2013, doi:10.4049/jimmunol.1202267 The Journal of Immunology Coordinated Changes in DNA Methylation in Antigen-Specific Memory CD4 T Cells Shin-ichi Hashimoto,*,†,‡ Katsumi Ogoshi,* Atsushi Sasaki,† Jun Abe,* Wei Qu,† Yoichiro Nakatani,† Budrul Ahsan,x Kenshiro Oshima,† Francis H. -
(P -Value<0.05, Fold Change≥1.4), 4 Vs. 0 Gy Irradiation
Table S1: Significant differentially expressed genes (P -Value<0.05, Fold Change≥1.4), 4 vs. 0 Gy irradiation Genbank Fold Change P -Value Gene Symbol Description Accession Q9F8M7_CARHY (Q9F8M7) DTDP-glucose 4,6-dehydratase (Fragment), partial (9%) 6.70 0.017399678 THC2699065 [THC2719287] 5.53 0.003379195 BC013657 BC013657 Homo sapiens cDNA clone IMAGE:4152983, partial cds. [BC013657] 5.10 0.024641735 THC2750781 Ciliary dynein heavy chain 5 (Axonemal beta dynein heavy chain 5) (HL1). 4.07 0.04353262 DNAH5 [Source:Uniprot/SWISSPROT;Acc:Q8TE73] [ENST00000382416] 3.81 0.002855909 NM_145263 SPATA18 Homo sapiens spermatogenesis associated 18 homolog (rat) (SPATA18), mRNA [NM_145263] AA418814 zw01a02.s1 Soares_NhHMPu_S1 Homo sapiens cDNA clone IMAGE:767978 3', 3.69 0.03203913 AA418814 AA418814 mRNA sequence [AA418814] AL356953 leucine-rich repeat-containing G protein-coupled receptor 6 {Homo sapiens} (exp=0; 3.63 0.0277936 THC2705989 wgp=1; cg=0), partial (4%) [THC2752981] AA484677 ne64a07.s1 NCI_CGAP_Alv1 Homo sapiens cDNA clone IMAGE:909012, mRNA 3.63 0.027098073 AA484677 AA484677 sequence [AA484677] oe06h09.s1 NCI_CGAP_Ov2 Homo sapiens cDNA clone IMAGE:1385153, mRNA sequence 3.48 0.04468495 AA837799 AA837799 [AA837799] Homo sapiens hypothetical protein LOC340109, mRNA (cDNA clone IMAGE:5578073), partial 3.27 0.031178378 BC039509 LOC643401 cds. [BC039509] Homo sapiens Fas (TNF receptor superfamily, member 6) (FAS), transcript variant 1, mRNA 3.24 0.022156298 NM_000043 FAS [NM_000043] 3.20 0.021043295 A_32_P125056 BF803942 CM2-CI0135-021100-477-g08 CI0135 Homo sapiens cDNA, mRNA sequence 3.04 0.043389246 BF803942 BF803942 [BF803942] 3.03 0.002430239 NM_015920 RPS27L Homo sapiens ribosomal protein S27-like (RPS27L), mRNA [NM_015920] Homo sapiens tumor necrosis factor receptor superfamily, member 10c, decoy without an 2.98 0.021202829 NM_003841 TNFRSF10C intracellular domain (TNFRSF10C), mRNA [NM_003841] 2.97 0.03243901 AB002384 C6orf32 Homo sapiens mRNA for KIAA0386 gene, partial cds. -
Isoflurane Inhibits Dopaminergic Synaptic Vesicle Exocytosis Coupled to Cav2.1 and Cav2.2 in Rat Midbrain Neurons
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. Research Article: New Research | Neuronal Excitability Isoflurane inhibits dopaminergic synaptic vesicle exocytosis coupled to CaV2.1 and CaV2.2 in rat midbrain neurons Christina L. Torturo1,2, Zhen-Yu Zhou1, Timothy A. Ryan1,3 and Hugh C. Hemmings1,2 1Departments of Anesthesiology, Weill Cornell Medicine, New York, NY 10065 2Pharmacology, Weill Cornell Medicine, New York, NY 10065 3Biochemistry, Weill Cornell Medicine, New York, NY 10065 https://doi.org/10.1523/ENEURO.0278-18.2018 Received: 16 July 2018 Revised: 18 December 2018 Accepted: 21 December 2018 Published: 10 January 2019 Author Contributions: CLT, ZZ, TAR and HCH designed the research; CLT performed the research, TAR contributed unpublished reagents/analytic tools; CLT and ZZ analyzed the data; CLT, ZZ, TAR, and HCH wrote the paper. Funding: http://doi.org/10.13039/100000002HHS | National Institutes of Health (NIH) GM58055 Conflict of Interest: HCH: Editor-in-Chief of the British Journal of Anaesthesia; consultant for Elsevier. Funding Sources: NIH GM58055 Corresponding author: Hugh C. Hemmings, E-mail: [email protected] Cite as: eNeuro 2019; 10.1523/ENEURO.0278-18.2018 Alerts: Sign up at www.eneuro.org/alerts to receive customized email alerts when the fully formatted version of this article is published. Accepted manuscripts are peer-reviewed but have not been through the copyediting, formatting, or proofreading process. Copyright © 2019 Torturo et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. -
Genetic Testing Policy Number: PG0041 ADVANTAGE | ELITE | HMO Last Review: 04/11/2021
Genetic Testing Policy Number: PG0041 ADVANTAGE | ELITE | HMO Last Review: 04/11/2021 INDIVIDUAL MARKETPLACE | PROMEDICA MEDICARE PLAN | PPO GUIDELINES This policy does not certify benefits or authorization of benefits, which is designated by each individual policyholder terms, conditions, exclusions and limitations contract. It does not constitute a contract or guarantee regarding coverage or reimbursement/payment. Paramount applies coding edits to all medical claims through coding logic software to evaluate the accuracy and adherence to accepted national standards. This medical policy is solely for guiding medical necessity and explaining correct procedure reporting used to assist in making coverage decisions and administering benefits. SCOPE X Professional X Facility DESCRIPTION A genetic test is the analysis of human DNA, RNA, chromosomes, proteins, or certain metabolites in order to detect alterations related to a heritable or acquired disorder. This can be accomplished by directly examining the DNA or RNA that makes up a gene (direct testing), looking at markers co-inherited with a disease-causing gene (linkage testing), assaying certain metabolites (biochemical testing), or examining the chromosomes (cytogenetic testing). Clinical genetic tests are those in which specimens are examined and results reported to the provider or patient for the purpose of diagnosis, prevention or treatment in the care of individual patients. Genetic testing is performed for a variety of intended uses: Diagnostic testing (to diagnose disease) Predictive -
Conference Schedule
Society on NeuroImmune Pharmacology (SNIP) 23rd Scientific Conference Hotel DOUBLETREE BY HILTON PHILADELPHIA CENTER CITY Philadelphia, PA, USA March 29 - April 1, 2017 Previous Conferences:1993 Toronto Hilton, Canada; 1994 Breakers, Palm Beach, FL; 1995 Bristol Court, San Diego, CA; 1996 Caribe Hilton, San Juan, PR; 1997 Opryland Hotel, Nashville TN; 1998 Scottsdale Princess, Scottsdale, AR; 2000 NIH Mazur Auditorium, Bethesda MD; 2001 Emory University, Atlanta, GA; 2002 Clearwater Beach Hilton, Clear Water, FL; 2004, La Fonda Hotel, Santa Fe, NM; 2005 Clearwater Beach Hilton, Clear Water, FL; 2006 La Fonda Hotel, Santa Fe, NM; 2007 City Center Marriott Hotel, Salt Lake City, UT; 2008 Francis Marion Hotel, Charleston, SC; 2009 Pearl Plaza Howard Johnson, Wuhan, China; 2010 Manhattan Beach Marriott, Manhattan Beach, CA; 2011 Hilton Clearwater Beach Resort, Clear Water Beach, FL; 2012 Hawaii Prince Hotel, Honolulu, HI; 2013 Conrad Hilton, San Juan, PR; 2014 Intercontinental New Orleans, LA.; 2015; Hyatt Regency, Miami, FL; 2016, Hotel Galaxy, Krakow, Poland. Page 1 TABLE OF CONTENTS Title Page 1 Table of Contents 2 Acknowledgement of Special Contributors and Sponsors 3-5 The SNIP Council, Officials, and Committees 6-7 Annual Society Awards 8-9 2016 Early Career Investigator Travel Awardees 9-11 2016 Plenary Speaker Biographies 12-14 Conference Agenda Wednesday March 29, 2017 City-Wide NeuroAIDS Discussion Group 15-16 Opening Reception 16 Poster Session 1 (W1-72, Abstract listings page 25) 16 1st Annual DISC Networking Hour 16 Thursday March 30, 2017 Presidential Symposium: Dopamine Neurotransmission in HIV-1 Infection 16-17 Presidential Symposium: Dr. David Sulzer 17 Symposium 2: Novel mechanisms of CNS infection 17-18 Meet the Mentors Lunch 18 SNIP Council Meeting 18 Pharmacology Symposium: Dr.