Acute and Long-Term Effects on Gene Expression and Behaviour
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Peripheral Nervous System……………………………………………….9
PhD School in Integrative Biomedical Research Department of Pharmacological and Biomolecular Sciences Curriculum: Neuroscience Molecular basis for the development of innovative therapies for peripheral neuropathies treatment: role and cross-regulation of the GABAergic system and neuroactive steroids SDD BIO/09 - Physiology Luca Franco Castelnovo Badge number R10402 PhD Tutor: Prof. Valerio Magnaghi PhD School Coordinator: Prof. Chiarella Sforza Academic year 2015/2016 INDEX Abstract…………………………………………………………………...page 1 Abbreviations list…………………………………………………………….....5 Introduction………………………………………………………………….....8 Peripheral nervous system……………………………………………….9 General concepts……………...……….……………………………........……..9 Sensory system and nociceptive fibers.………………..………….…………..12 Schwann cells and myelination……….……..………………...………………15 Peripheral neuropathies…….…………………………………………...26 General concepts……………………………………………………...……….26 Neuropathic pain……………………………………...……………………….27 Nerve regeneration…………………………………………………………….28 The GABAergic system………….……………………………………...32 GABA……………….…………………………………………………..……..32 GABA-A receptors…………………………………………………………….33 GABA-B receptors…………………………………………………………….42 GABAergic system in the peripheral nervous system…………………………47 Protein kinase C – type ε……………………….………………………..51 General concepts…………………………………………………….…………51 Cross-talk with allopregnanolone and GABA-A………………………………54 Neuroactive steroids…………......………………………………………57 General concepts…………………………………….…………………………57 Mechanism of action…………………………….……………………………..59 Progesterone derivatives………………………………….……………………60 -
Molecular Genetic Analysis of Two Loci (Ity2 and Ity3) Involved in The
Copyright Ó 2007 by the Genetics Society of America DOI: 10.1534/genetics.107.075523 Molecular Genetic Analysis of Two Loci (Ity2 and Ity3) Involved in the Host Response to Infection With Salmonella Typhimurium Using Congenic Mice and Expression Profiling Vanessa Sancho-Shimizu,*,† Rabia Khan,*,† Serge Mostowy,† Line Larivie`re,† Rosalie Wilkinson,† Noe´mie Riendeau,† Marcel Behr† and Danielle Malo*,†,‡,1 *Department of Human Genetics, McGill University, Montreal, Quebec H3G 1A4, Canada and †Center for the Study of Host Resistance, McGill University Health Center, Montreal, Quebec H3G 1A4, Canada and ‡Department of Medicine, McGill University, Montreal, Quebec H3G 1A4, Canada Manuscript received May 4, 2007 Accepted for publication July 27, 2007 ABSTRACT Numerous genes have been identified to date that contribute to the host response to systemic Sal- monella Typhimurium infection in mice. We have previously identified two loci, Ity2 and Ity3, that control survival to Salmonella infection in the wild-derived inbred MOLF/Ei mouse using a (C57BL/6J 3 MOLF/ Ei)F2cross. We validated the existence of these two loci by creating congenic mice carrying each quan- titative trait locus (QTL) in isolation. Subcongenic mice generated for each locus allowed us to define the critical intervals underlying Ity2 and Ity3. Furthermore, expression profiling was carried out with the aim of identifying differentially expressed genes within the critical intervals as potential candidate genes. Genomewide expression arrays were used to interrogate expression differences in the Ity2 congenics, leading to the identification of a new candidate gene (Havcr2, hepatitis A virus cellular receptor 2). Interval-specific oligonucleotide arrays were created for Ity3, identifying one potential candidate gene (Chi3l1, chitinase 3-like 1) to be pursued further. -
Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex
Nicotinic Signalling and Neurosteroid Modulation in Principal Neurons of the Hippocampal Formation and Prefrontal Cortex by Beryl Yik Ting Chung A Thesis presented to The University of Guelph In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences and Neuroscience Guelph, Ontario, Canada © Beryl Yik Ting Chung, April, 2018 ABSTRACT NICOTINIC SIGNALLING AND NEUROSTEROID MODULATION IN PRINCIPAL NEURONS OF THE HIPPOCAMPAL FORMATION AND PREFRONTAL CORTEX Beryl Yik Ting Chung Advisor: University of Guelph, 2018 Dr. Craig D.C. Bailey Nicotinic signalling plays an important role in coordinating the response of neuronal networks in many brain regions. During pre- and postnatal circuit formation, neurotransmission mediated by nicotinic acetylcholine receptors (nAChRs) influences neuronal survival and regulates neuronal excitability, synaptic transmission, and synaptic plasticity. Nicotinic signalling is also necessary for the proper function of the hippocampal formation (HF) and prefrontal cortex (PFC), which are anatomically and functionally connected and facilitate higher-order cognitive functions. The decline or dysfunction in nicotinic signalling and nAChR function has been observed in various neurological disorders, and the disruption or alteration of nicotinic signalling in the HF and/or PFC can impair learning and memory. While the location and functional role of the α4β2* nAChR isoform has been well characterized in the medial portion of the PFC, this is not well-established in the HF. What is the role of α4β2* nAChRs in excitatory principal neurons of the HF during early development? Growing evidence suggests that the progesterone metabolite allopregnanolone (ALLO) plays a role in mediating the proper function of the HF and the PFC, and that it may also inhibit nAChR function. -
Establishing the Pathogenicity of Novel Mitochondrial DNA Sequence Variations: a Cell and Molecular Biology Approach
Mafalda Rita Avó Bacalhau Establishing the Pathogenicity of Novel Mitochondrial DNA Sequence Variations: a Cell and Molecular Biology Approach Tese de doutoramento do Programa de Doutoramento em Ciências da Saúde, ramo de Ciências Biomédicas, orientada pela Professora Doutora Maria Manuela Monteiro Grazina e co-orientada pelo Professor Doutor Henrique Manuel Paixão dos Santos Girão e pela Professora Doutora Lee-Jun C. Wong e apresentada à Faculdade de Medicina da Universidade de Coimbra Julho 2017 Faculty of Medicine Establishing the pathogenicity of novel mitochondrial DNA sequence variations: a cell and molecular biology approach Mafalda Rita Avó Bacalhau Tese de doutoramento do programa em Ciências da Saúde, ramo de Ciências Biomédicas, realizada sob a orientação científica da Professora Doutora Maria Manuela Monteiro Grazina; e co-orientação do Professor Doutor Henrique Manuel Paixão dos Santos Girão e da Professora Doutora Lee-Jun C. Wong, apresentada à Faculdade de Medicina da Universidade de Coimbra. Julho, 2017 Copyright© Mafalda Bacalhau e Manuela Grazina, 2017 Esta cópia da tese é fornecida na condição de que quem a consulta reconhece que os direitos de autor são pertença do autor da tese e do orientador científico e que nenhuma citação ou informação obtida a partir dela pode ser publicada sem a referência apropriada e autorização. This copy of the thesis has been supplied on the condition that anyone who consults it recognizes that its copyright belongs to its author and scientific supervisor and that no quotation from the -
Frontiers in Integrative Genomics and Translational Bioinformatics
BioMed Research International Frontiers in Integrative Genomics and Translational Bioinformatics Guest Editors: Zhongming Zhao, Victor X. Jin, Yufei Huang, Chittibabu Guda, and Jianhua Ruan Frontiers in Integrative Genomics and Translational Bioinformatics BioMed Research International Frontiers in Integrative Genomics and Translational Bioinformatics Guest Editors: Zhongming Zhao, Victor X. Jin, Yufei Huang, Chittibabu Guda, and Jianhua Ruan Copyright © òýÔ Hindawi Publishing Corporation. All rights reserved. is is a special issue published in “BioMed Research International.” All articles are open access articles distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Contents Frontiers in Integrative Genomics and Translational Bioinformatics, Zhongming Zhao, Victor X. Jin, Yufei Huang, Chittibabu Guda, and Jianhua Ruan Volume òýÔ , Article ID Þò ¥ÀÔ, ç pages Building Integrated Ontological Knowledge Structures with Ecient Approximation Algorithms, Yang Xiang and Sarath Chandra Janga Volume òýÔ , Article ID ýÔ ò, Ô¥ pages Predicting Drug-Target Interactions via Within-Score and Between-Score, Jian-Yu Shi, Zun Liu, Hui Yu, and Yong-Jun Li Volume òýÔ , Article ID ç ýÀç, À pages RNAseq by Total RNA Library Identies Additional RNAs Compared to Poly(A) RNA Library, Yan Guo, Shilin Zhao, Quanhu Sheng, Mingsheng Guo, Brian Lehmann, Jennifer Pietenpol, David C. Samuels, and Yu Shyr Volume òýÔ , Article ID âòÔçý, À pages Construction of Pancreatic Cancer Classier Based on SVM Optimized by Improved FOA, Huiyan Jiang, Di Zhao, Ruiping Zheng, and Xiaoqi Ma Volume òýÔ , Article ID ÞÔýòç, Ôò pages OperomeDB: A Database of Condition-Specic Transcription Units in Prokaryotic Genomes, Kashish Chetal and Sarath Chandra Janga Volume òýÔ , Article ID çÔòÔÞ, Ôý pages How to Choose In Vitro Systems to Predict In Vivo Drug Clearance: A System Pharmacology Perspective, Lei Wang, ChienWei Chiang, Hong Liang, Hengyi Wu, Weixing Feng, Sara K. -
A Genome‐Wide Association Study Highlights a Regulatory Role for IFNG‐AS1
bioRxiv preprint doi: https://doi.org/10.1101/2020.01.13.903989; this version posted January 14, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. A genome‐wide association study highlights a regulatory role for IFNG‐AS1 contributing to cutaneous leishmaniasis in Brazil Short title: A GWAS for cutaneous leishmaniasis in Brazil Léa C. Castellucci1,2,*, Lucas Almeida1,2,*, Svetlana Cherlin3,*, Michaela Fakiola4, Edgar Carvalho1, Amanda B. Figueiredo5, Clara M. Cavalcanti5, Natalia S. Alves5, Walderez O. Dutra1,6 , Kenneth J. Gollob1,5,7, Heather J. Cordell3 , and Jenefer M. Blackwell8,9 *Equal contributions 1National Institute of Science and Technology in Tropical Diseases, Brazil; 2Federal University of Bahia, Salvador, Brazil; 3Population Health Sciences Institute, Newcastle University, UK; 4INGM‐National Institute of Molecular Genetics "Romeo ed Enrica Invernizzi" Milan, Milan, Italy; 5International Center for Research, AC Camargo Cancer Center, São Paulo, Brazil; 6Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil; 7Núcleo de Ensino e Pesquisa, Instituto Mario Penna, Belo Horizonte, Brazil; 8Department of Pathology, University of Cambridge, UK; 9Telethon Kids Institute, The University of Western Australia, Western Australia Corresponding author: Jenefer M. Blackwell ([email protected] Correspondence to: Jenefer M. Blackwell, PO Box 855, West Perth, Western Australia 6872; Hospital Avenue, Nedlands, Western Australia 6009; Phone: +61 8 63191000. Funding British Medical Research Council (MRC) MR/N017390/1, FAPEMIG grant in cooperation with MRC/CONFAP (CBB-APQ-00883-16), National Institute of Science and Technology in Tropical Diseases, Brazil (N° 573839/2008–5), CNPq (K.J.G. -
Genomic and Expression Profiling of Chromosome 17 in Breast Cancer Reveals Complex Patterns of Alterations and Novel Candidate Genes
[CANCER RESEARCH 64, 6453–6460, September 15, 2004] Genomic and Expression Profiling of Chromosome 17 in Breast Cancer Reveals Complex Patterns of Alterations and Novel Candidate Genes Be´atrice Orsetti,1 Me´lanie Nugoli,1 Nathalie Cervera,1 Laurence Lasorsa,1 Paul Chuchana,1 Lisa Ursule,1 Catherine Nguyen,2 Richard Redon,3 Stanislas du Manoir,3 Carmen Rodriguez,1 and Charles Theillet1 1Ge´notypes et Phe´notypes Tumoraux, EMI229 INSERM/Universite´ Montpellier I, Montpellier, France; 2ERM 206 INSERM/Universite´ Aix-Marseille 2, Parc Scientifique de Luminy, Marseille cedex, France; and 3IGBMC, U596 INSERM/Universite´Louis Pasteur, Parc d’Innovation, Illkirch cedex, France ABSTRACT 17q12-q21 corresponding to the amplification of ERBB2 and collinear genes, and a large region at 17q23 (5, 6). A number of new candidate Chromosome 17 is severely rearranged in breast cancer. Whereas the oncogenes have been identified, among which GRB7 and TOP2A at short arm undergoes frequent losses, the long arm harbors complex 17q21 or RP6SKB1, TBX2, PPM1D, and MUL at 17q23 have drawn combinations of gains and losses. In this work we present a comprehensive study of quantitative anomalies at chromosome 17 by genomic array- most attention (6–10). Furthermore, DNA microarray studies have comparative genomic hybridization and of associated RNA expression revealed additional candidates, with some located outside current changes by cDNA arrays. We built a genomic array covering the entire regions of gains, thus suggesting the existence of additional amplicons chromosome at an average density of 1 clone per 0.5 Mb, and patterns of on 17q (8, 9). gains and losses were characterized in 30 breast cancer cell lines and 22 Our previous loss of heterozygosity mapping data pointed to the primary tumors. -
Computational and Experimental Approaches for Evaluating the Genetic Basis of Mitochondrial Disorders
Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Lieber, Daniel Solomon. 2013. Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders. Doctoral dissertation, Harvard University. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11158264 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 Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders A dissertation presented by Daniel Solomon Lieber to The Committee on Higher Degrees in Systems Biology in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Systems Biology Harvard University Cambridge, Massachusetts April 2013 © 2013 - Daniel Solomon Lieber All rights reserved. Dissertation Adviser: Professor Vamsi K. Mootha Daniel Solomon Lieber Computational and Experimental Approaches For Evaluating the Genetic Basis of Mitochondrial Disorders Abstract Mitochondria are responsible for some of the cell’s most fundamental biological pathways and metabolic processes, including aerobic ATP production by the mitochondrial respiratory chain. In humans, mitochondrial dysfunction can lead to severe disorders of energy metabolism, which are collectively referred to as mitochondrial disorders and affect approximately 1:5,000 individuals. These disorders are clinically heterogeneous and can affect multiple organ systems, often within a single individual. Symptoms can include myopathy, exercise intolerance, hearing loss, blindness, stroke, seizures, diabetes, and GI dysmotility. -
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement. -
Whole Exome Sequencing in Families at High Risk for Hodgkin Lymphoma: Identification of a Predisposing Mutation in the KDR Gene
Hodgkin Lymphoma SUPPLEMENTARY APPENDIX Whole exome sequencing in families at high risk for Hodgkin lymphoma: identification of a predisposing mutation in the KDR gene Melissa Rotunno, 1 Mary L. McMaster, 1 Joseph Boland, 2 Sara Bass, 2 Xijun Zhang, 2 Laurie Burdett, 2 Belynda Hicks, 2 Sarangan Ravichandran, 3 Brian T. Luke, 3 Meredith Yeager, 2 Laura Fontaine, 4 Paula L. Hyland, 1 Alisa M. Goldstein, 1 NCI DCEG Cancer Sequencing Working Group, NCI DCEG Cancer Genomics Research Laboratory, Stephen J. Chanock, 5 Neil E. Caporaso, 1 Margaret A. Tucker, 6 and Lynn R. Goldin 1 1Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 2Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; 3Ad - vanced Biomedical Computing Center, Leidos Biomedical Research Inc.; Frederick National Laboratory for Cancer Research, Frederick, MD; 4Westat, Inc., Rockville MD; 5Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD; and 6Human Genetics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA ©2016 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol.2015.135475 Received: August 19, 2015. Accepted: January 7, 2016. Pre-published: June 13, 2016. Correspondence: [email protected] Supplemental Author Information: NCI DCEG Cancer Sequencing Working Group: Mark H. Greene, Allan Hildesheim, Nan Hu, Maria Theresa Landi, Jennifer Loud, Phuong Mai, Lisa Mirabello, Lindsay Morton, Dilys Parry, Anand Pathak, Douglas R. Stewart, Philip R. Taylor, Geoffrey S. Tobias, Xiaohong R. Yang, Guoqin Yu NCI DCEG Cancer Genomics Research Laboratory: Salma Chowdhury, Michael Cullen, Casey Dagnall, Herbert Higson, Amy A. -
PRODUCT SPECIFICATION Anti-PAQR9 Product
Anti-PAQR9 Product Datasheet Polyclonal Antibody PRODUCT SPECIFICATION Product Name Anti-PAQR9 Product Number HPA052798 Gene Description progestin and adipoQ receptor family member IX Clonality Polyclonal Isotype IgG Host Rabbit Antigen Sequence Recombinant Protein Epitope Signature Tag (PrEST) antigen sequence: IMLESWLFDLRGENPTLFVHF Purification Method Affinity purified using the PrEST antigen as affinity ligand Verified Species Human Reactivity Recommended IHC (Immunohistochemistry) Applications - Antibody dilution: 1:20 - 1:50 - Retrieval method: HIER pH6 Characterization Data Available at atlasantibodies.com/products/HPA052798 Buffer 40% glycerol and PBS (pH 7.2). 0.02% sodium azide is added as preservative. Concentration Lot dependent Storage Store at +4°C for short term storage. Long time storage is recommended at -20°C. Notes Gently mix before use. Optimal concentrations and conditions for each application should be determined by the user. For protocols, additional product information, such as images and references, see atlasantibodies.com. Product of Sweden. For research use only. Not intended for pharmaceutical development, diagnostic, therapeutic or any in vivo use. No products from Atlas Antibodies may be resold, modified for resale or used to manufacture commercial products without prior written approval from Atlas Antibodies AB. Warranty: The products supplied by Atlas Antibodies are warranted to meet stated product specifications and to conform to label descriptions when used and stored properly. Unless otherwise stated, this warranty is limited to one year from date of sales for products used, handled and stored according to Atlas Antibodies AB's instructions. Atlas Antibodies AB's sole liability is limited to replacement of the product or refund of the purchase price. -
CRLF3 (D-10): Sc-398388
SANTA CRUZ BIOTECHNOLOGY, INC. CRLF3 (D-10): sc-398388 BACKGROUND APPLICATIONS CRLF3 (cytokine receptor-like factor 3), also known as type I cytokine receptor CRLF3 (D-10) is recommended for detection of CRLF3 of mouse, rat and like factor, FRWS, CREME9 (cytokine receptor-like molecule 9), CYTOR4 (cyto- human origin by Western Blotting (starting dilution 1:100, dilution range kine receptor-related protein 4) or P48 (type I cytokine receptor-like factor p48), 1:100-1:1000), immunoprecipitation [1-2 µg per 100-500 µg of total protein is a 442 amino acid protein that contains one fibronectin type-III domain. (1 ml of cell lysate)], immunofluorescence (starting dilution 1:50, dilution CRLF3 is expressed in lesion actinic keratosis (AK) and skin and squamous range 1:50-1:500) and solid phase ELISA (starting dilution 1:30, dilution cell carcinoma (SCC), and is thought to negatively regulate the G0/G1 phase range 1:30-1:3000). of the cell cycle. The gene encoding CRLF3 maps to human chromosome 17, Suitable for use as control antibody for CRLF3 siRNA (h): sc-94066, CRLF3 which comprises over 2.5% of the human genome and encodes over 1,200 siRNA (m): sc-142577, CRLF3 shRNA Plasmid (h): sc-94066-SH, CRLF3 shRNA genes. Two key tumor suppressor genes are associated with chromosome 17, Plasmid (m): sc-142577-SH, CRLF3 shRNA (h) Lentiviral Particles: sc-94066-V namely, p53 and BRCA1. Malfunction or loss of p53 expression is associated and CRLF3 shRNA (m) Lentiviral Particles: sc-142577-V. with malignant cell growth and Li-Fraumeni syndrome.