DOCSLIB.ORG

ION CHANNEL RECEPTORS TÁMOP-4.1.2-08/1/A-2009-0011 Ion Channel Receptors

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
ION CHANNEL RECEPTORS TÁMOP-4.1.2-08/1/A-2009-0011 Ion Channel Receptors Manifestation of Novel Social Challenges of the European Union in the Teaching Material of Medical Biotechnology Master’s Programmes at the University of Pécs and at the University of Debrecen Identification number: TÁMOP-4.1.2-08/1/A-2009-0011 Manifestation of Novel Social Challenges of the European Union in the Teaching Material of Medical Biotechnology Master’s Programmes at the University of Pécs and at the University of Debrecen Identification number: TÁMOP-4.1.2-08/1/A-2009-0011 Tímea Berki and Ferenc Boldizsár Signal transduction ION CHANNEL RECEPTORS TÁMOP-4.1.2-08/1/A-2009-0011 Ion channel receptors 1 Cys-loop receptors: pentameric structure, 4 transmembrane (TM) regions/subunit – Acetylcholin (Ach) Nicotinic R – Na+ channel - – GABAA, GABAC, Glycine – Cl channels (inhibitory role in CNS) 2 Glutamate-activated cationic channels: (excitatory role in CNS), tetrameric stucture, 3 TM regions/subunit – eg. iGlu 3 ATP-gated channels: 3 homologous subunits, 2 TM regions/subunit – eg. P2X purinoreceptor TÁMOP-4.1.2-08/1/A-2009-0011 Cys-loop ion-channel receptors N Pore C C C N N N N C C TM TM TM TM 1 2 3 4 Receptor type GABAA GABAC Glycine g a b p2 p1 b a Subunit diversity a1-6, b1-3, g1-3, d,e,k, and q p1-3 a1-4, b TÁMOP-4.1.2-08/1/A-2009-0011 Vertebrate anionic Cys-loop receptors Type Class Protein name Gene Previous names a1 GABRA1 a2 GABRA2 a3 GABRA3 EJM, ECA4 alpha a4 GABRA4 a5 GABRA5 a6 GABRA6 b1 GABRB1 beta b2 GABRB2 ECA5 b3 GABRB3 g1 GABRG1 GABAA gamma g2 GABRG2 CAE2, ECA2, GEFSP3 g3 GABRG3 delta d GABRD epsilon e GABRE pi p GABRP theta q GABRQ GABRR rho r GABRR GABAC GABRR a1 GLRA1 a2 GLRA2 alpha STHE Glycine (GlyR) a3 GLRA3 a4 GLRA4 beta b GLRB TÁMOP-4.1.2-08/1/A-2009-0011 Vertebrate cationic Cys-loop receptors Type Class Protein name Gene Previous names 5-HT3A HTR3A 5-HT 5-HT3B HTR3B 3A 5-HT Serotonin 5-HT3C HTR3C 3B 5-HT3 5-HT (5-HT) 5-HT3D HTR3D 3C 5-HT 5-HT3E HTR3E 3D 5-HT 3E a1 CHRNA1 a2 CHRNA2 a3 CHRNA3 a4 CHRNA4 a5 CHRNA5 alpha ACHRA, ACHRD, CHRNA, CMS2A, FCCMS, SCCMS a6 CHRNA6 a7 CHRNA7 a8 CHRNA8 a9 CHRNA9 Nicotinic acetylcholine a10 CHRNA10 (nAChR) b1 CHRNB1 b2 CHRNB2 beta CMS2A, SCCMS, ACHRB, CHRNB, CMS1D, EFNL3, nAChRB2 b3 CHRNB3 b4 CHRNB4 gamma g CHRNG ACHRG delta d CHRND ACHRD, CMS2A, FCCMS, SCCMS epsilon e CHRNE ACHRE, CMS1D, CMS1E, CMS2A, FCCMS, SCCMS Zinc-activated ion ZAC ZACN ZAC1, L2m, LGICZ1 channel TÁMOP-4.1.2-08/1/A-2009-0011 Ionotropic glutamate receptors Type Class Protein name Gene Previous names GluA1 GRIA1 GLUA1, GluR1, GluRA, GluR-A, GluR-K1, HBGR1 GluA2 GRIA2 GLU , GluR2, GluRB, GluR-B, GluR-K2, HBGR2 AMPA GluA1 A2 GluA3 GRIA3 GLUA3, GluR3, GluRC, GluR-D, GluR-K3 GluA4 GRIA4 GLUA4, GluR4, GluRD, GluR-D GluK1 GRIK1 GLUK5, GluR5, GluR-5, EAA3 GluK2 GRIK2 GLUK6, GluR6, GluR-6, EAA4, Kainate GluK GluK3 GRIK3 GLUK7, GluR7, GluR-7, EAA5, GluK4 GRIK4 GLUK1, KA1, KA-1, EAA1 GluK5 GRI5 GLUK2, KA2, KA-2, EAA2 GluN1 GRIN1 GluN NRL1A GRINL1A GLUN1, NMDA-R1, NR1, GluRz1 NRL1B GRINL1B GluN2A GRIN2A GLUN2A, NMDA-R2A, NR2A, GluRe1 NMDA GluN2B GRIN2B GLUN2B, NMDA-R2B, NR2B, GluRe2 GluN2C GRIN2C GLUN2C, NMDA-R2C, NR2C, GluRe3 GluN2D GRIN2D GLUN2D, NMDA-R2D, NR2D, GluRe4 GluN3A GRIN3A GLUN3A, NMDA-R3A, NMDAR-L, chi-1 GluN3B GRIN3B GLUN3B, NMDA-R3B GluD1 GRID1 ‘Orphan’ (GluD) GluRd1 GluD2 GRID2 TÁMOP-4.1.2-08/1/A-2009-0011 Nicotinic Ach receptor • Pore formed from 5 subunits: 2a, b, g, d • Opening: the 2a units are distorted • Desensitization: in the open conformation the b, g, d subunits become phosphorylated by Protein kinase A and C Top Front TÁMOP-4.1.2-08/1/A-2009-0011 Common neurotransmitters Neurotransmitter Action Receptor subtypes Acetylcholine (Ach) +/- Nicotinic, Muscarinic Norepinephrine (NE) + α1/2, β1/2/3 Dopamine +/- D1-D4 Serotonin (5-HT) +/- 5-HT1A etc. Glutamate (Glu) + NMDA, AMPA GABA - GABAA, GABAB Encephalins - μ, κ, δ TÁMOP-4.1.2-08/1/A-2009-0011 Synapse between two neurons - neurotransmission Presynaptic neuron (axon terminal) Synaptic vesicles NT transporter Voltage-gated sodium channel + Neurotransmitter molecule Ligand-gated ion channel (direct Postsynaptic neuron excitation or GPCR + inhibition) (modulatory) TÁMOP-4.1.2-08/1/A-2009-0011 Neurotransmission Ions Neurotransmitter Plasma membrane Cytoplasm Ion channel Neurotransmitter Receptor Plasma membrane Cytoplasm a g a b Effector Intracellular GTP GTP protein messengers G-protein is activated G-protein subunits or intracellular messengers modulate ion channels TÁMOP-4.1.2-08/1/A-2009-0011 Neurotransmitters Acetylcholine Acetylcholine (motor neurons) m/i Indolamines Serotonin (memory, emotion) m/i Monoamines Dopamine (motivation, addiction) m Catecholamines Norepinephrine/Noradrenaline (sympathetic NS) m Epinephrine m Glutamate (most prominent in CNS, excitatory) m/i GABA (30%-40% of CNS synapses, inhibitory) m/i Amino Acids Aspartate i Glycine (can be excit. or inhib. depending on Cl- conc.) * i Adenosine m Guanosine m Purines ATP i/m Others Endorphins Opioids Enkephalins Dynorphins Neuropeptides Substance P Non-opioids Neuropeptide Y m Others NO Soluble gases CO TÁMOP-4.1.2-08/1/A-2009-0011 Acetylcholine receptors Stage 1 Stage 2 Stage 3 Nicotinic muscle Nicotinic Junctional [(a1)2bed] Phenyltrimethyl-ammonium Nicotinic Embyonic [(a1) bgd] Elapid a-toxins, d-Tubocurarine 2 Nicotinic Neuronal a2 (a-toxin insensitive) Nicotinic Nicotinic Neuronal b2 Nicotine Nicotinic Neuronal a3 (a-toxin insensitive) d-Tubocurarine Nicotinic Neuronal b3 Nicotinic Neuronal a4 (a-toxin insensitive) Nicotinic neuronal (a+b) Nicotinic Neuronal b4 Dimethylphenyl-piperazinuim, Cystine Nicotinic Neuronal a5 (a-toxin insensitive) Trimethaphan Nicotinic Neuronal b5 Neuronal bungarotoxin Cholinergic Nicotinic Neuronal a5 (non-functional without a subunits) Acetylcholine Nicotinic Neuronal a6 (a-toxin insensitive) Nicotinic Neuronal a7 (a-toxin sensitive) Nicotinic Neuronal a8 (a-toxin sensitive) Nicotinic Neuronal a9 Muscarinic m1-M1 Pirenzepine Muscarinic m2-M2 Methoctramine Muscarinic Oxotremorine Muscarine, Pilocarpine Propyllbenzilylcholine mustard Muscarinic m4-M4 Himbacine Atropine Quinuclidinyl benzilate Muscarinic m3-M3 Hexahydro-siladifenidol Muscarinic m5-M5 TÁMOP-4.1.2-08/1/A-2009-0011 Acetylcholin-esterase (AchE): • Quick removal of Ach from the synaptic space • Ach → choline+acetyl • Reversible inhibitors: therapeutic use (myasthenia, glaucoma, Alzheimer’s) • Irreversible inhibitors: chemical weapons and pesticides eg. organophosphates Ach AchE .
Load more

Recommended publications
  • Release Β ATP-Induced IL-1 and Canonical Nicotinic Agonists Inhibit Phosphocholine-Modified Macromolecules
    Phosphocholine-Modified Macromolecules and Canonical Nicotinic Agonists Inhibit ATP-Induced IL-1β Release This information is current as Andreas Hecker, Mira Küllmar, Sigrid Wilker, Katrin of September 24, 2021. Richter, Anna Zakrzewicz, Srebrena Atanasova, Verena Mathes, Thomas Timm, Sabrina Lerner, Jochen Klein, Andreas Kaufmann, Stefan Bauer, Winfried Padberg, Wolfgang Kummer, Sabina Janciauskiene, Martin Fronius, Elke K. H. Schweda, Günter Lochnit and Veronika Grau Downloaded from J Immunol 2015; 195:2325-2334; Prepublished online 22 July 2015; doi: 10.4049/jimmunol.1400974 http://www.jimmunol.org/content/195/5/2325 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2015/07/22/jimmunol.140097 Material 4.DCSupplemental References This article cites 42 articles, 11 of which you can access for free at: http://www.jimmunol.org/content/195/5/2325.full#ref-list-1 by guest on September 24, 2021 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2015 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606.
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Download Download
    Supplementary Figure S1. Results of flow cytometry analysis, performed to estimate CD34 positivity, after immunomagnetic separation in two different experiments. As monoclonal antibody for labeling the sample, the fluorescein isothiocyanate (FITC)- conjugated mouse anti-human CD34 MoAb (Mylteni) was used. Briefly, cell samples were incubated in the presence of the indicated MoAbs, at the proper dilution, in PBS containing 5% FCS and 1% Fc receptor (FcR) blocking reagent (Miltenyi) for 30 min at 4 C. Cells were then washed twice, resuspended with PBS and analyzed by a Coulter Epics XL (Coulter Electronics Inc., Hialeah, FL, USA) flow cytometer. only use Non-commercial 1 Supplementary Table S1. Complete list of the datasets used in this study and their sources. GEO Total samples Geo selected GEO accession of used Platform Reference series in series samples samples GSM142565 GSM142566 GSM142567 GSM142568 GSE6146 HG-U133A 14 8 - GSM142569 GSM142571 GSM142572 GSM142574 GSM51391 GSM51392 GSE2666 HG-U133A 36 4 1 GSM51393 GSM51394 only GSM321583 GSE12803 HG-U133A 20 3 GSM321584 2 GSM321585 use Promyelocytes_1 Promyelocytes_2 Promyelocytes_3 Promyelocytes_4 HG-U133A 8 8 3 GSE64282 Promyelocytes_5 Promyelocytes_6 Promyelocytes_7 Promyelocytes_8 Non-commercial 2 Supplementary Table S2. Chromosomal regions up-regulated in CD34+ samples as identified by the LAP procedure with the two-class statistics coded in the PREDA R package and an FDR threshold of 0.5. Functional enrichment analysis has been performed using DAVID (http://david.abcc.ncifcrf.gov/)
    [Show full text]
  • Understanding the Role of the Chromosome 15Q25.1 in COPD Through Epigenetics and Transcriptomics
    European Journal of Human Genetics (2018) 26:709–722 https://doi.org/10.1038/s41431-017-0089-8 ARTICLE Understanding the role of the chromosome 15q25.1 in COPD through epigenetics and transcriptomics 1 1,2 1,3,4 5,6 5,6 Ivana Nedeljkovic ● Elena Carnero-Montoro ● Lies Lahousse ● Diana A. van der Plaat ● Kim de Jong ● 5,6 5,7 6 8 9 10 Judith M. Vonk ● Cleo C. van Diemen ● Alen Faiz ● Maarten van den Berge ● Ma’en Obeidat ● Yohan Bossé ● 11 1,12 12 1 David C. Nickle ● BIOS Consortium ● Andre G. Uitterlinden ● Joyce J. B. van Meurs ● Bruno C. H. Stricker ● 1,4,13 6,8 5,6 1 1 Guy G. Brusselle ● Dirkje S. Postma ● H. Marike Boezen ● Cornelia M. van Duijn ● Najaf Amin Received: 14 March 2017 / Revised: 6 November 2017 / Accepted: 19 December 2017 / Published online: 8 February 2018 © The Author(s) 2018. This article is published with open access Abstract Chronic obstructive pulmonary disease (COPD) is a major health burden in adults and cigarette smoking is considered the most important environmental risk factor of COPD. Chromosome 15q25.1 locus is associated with both COPD and smoking. Our study aims at understanding the mechanism underlying the association of chromosome 15q25.1 with COPD through epigenetic and transcriptional variation in a population-based setting. To assess if COPD-associated variants in 1234567890();,: 15q25.1 are methylation quantitative trait loci, epigenome-wide association analysis of four genetic variants, previously associated with COPD (P < 5 × 10−8) in the 15q25.1 locus (rs12914385:C>T-CHRNA3, rs8034191:T>C-HYKK, rs13180: C>T-IREB2 and rs8042238:C>T-IREB2), was performed in the Rotterdam study (n = 1489).
    [Show full text]
  • Supplementary Data
    Supplementary Methods Mutation and microdeletion screening by high resolution melting High-throughput mutation screening of DIS3L2 exons 1-16 and HDAC4 was performed by Lightscanner high resolution melting analysis (Idaho Technology, Salt Lake City, UT). Exons 17-21 of DIS3L2 were not sequenced due to an apparent genomic duplication and consequent inability to uniquely amplify these exons. DNA samples were amplified using LightScanner mastermix under the manufacturer’s guidelines (Idaho Technology). After PCR, samples were heated at 0.1°C/s in the Lightscanner instrument and fluorescence was collected from 60 to 95°C. Melting curves were analyzed using LightScanner software (v2.0, Idaho Technology). Microdeletion screening across DIS3L2 was performed on paired normal- tumor samples using Lightscanner Lunaprobe SNP genotyping. Seven SNPs, ~60 Kb apart (rs2679184, rs12988522, rs4973500, rs3100586, rs3116179, rs923333 and rs2633254) were amplified in separate reactions and analyzed as above. Detailed conditions and primer/probe sequences are available on request. Variant amplicons were sequenced as described below. Direct sequencing was also performed for all exons where a common polymorphism might mask detection of a mutation by Lightscanner. Samples with known LOH were analyzed entirely by direct sequencing, since Lightscanner detects altered melting profiles of DNA heteroduplexes and these cannot exist in hemizygous samples. Sequencing of candidate genes Direct sequencing of exons and flanking consensus splice signals was performed for DIS3L2, GIGYF2, NPPC, HDAC4, TWIST2 and miR-562. PCR amplification was performed using HotStarTaq Mastermix and Q solution (Qiagen, Valencia, CA); all conditions and primers are available on request. PCR products were treated with shrimp alkaline phosphatase and exonuclease-I (New England Biolabs, Ipswich, MA) and sequenced using BigDye terminator chemistry on a 3730xl sequencer (Applied Biosystems, Foster City, CA).
    [Show full text]
  • Scrutiny of the CHRNA5-CHRNA3-CHRNB4
    Washington University School of Medicine Digital Commons@Becker Open Access Publications 2013 Scrutiny of the CHRNA5-CHRNA3-CHRNB4 smoking behavior locus reveals a novel association with alcohol use in a Finnish population based study Jenni Hällfors University of Helsinki Anu Loukola University of Helsinki Janne Pitkäniemi University of Helsinki Ulla Broms University of Helsinki Satu Männistö National Institute for Health and Welfare, Helsinki, Finland See next page for additional authors Follow this and additional works at: https://digitalcommons.wustl.edu/open_access_pubs Recommended Citation Hällfors, Jenni; Loukola, Anu; Pitkäniemi, Janne; Broms, Ulla; Männistö, Satu; Salomaa, Veikko; Heliövaara, Markku; Lehtimäki, Terho; Raitakari, Olli; Madden, Pamela AF; Heath, Andrew C.; Montgomery, Grant W.; Martin, Nicholas G.; Korhonen, Tellervo; and Kaprio, Jaakko, ,"Scrutiny of the CHRNA5-CHRNA3-CHRNB4 smoking behavior locus reveals a novel association with alcohol use in a Finnish population based study." International Journal of Molecular Epidemiology and Genetics.4,2. 109-119. (2013). https://digitalcommons.wustl.edu/open_access_pubs/3075 This Open Access Publication is brought to you for free and open access by Digital Commons@Becker. It has been accepted for inclusion in Open Access Publications by an authorized administrator of Digital Commons@Becker. For more information, please contact [email protected]. Authors Jenni Hällfors, Anu Loukola, Janne Pitkäniemi, Ulla Broms, Satu Männistö, Veikko Salomaa, Markku Heliövaara, Terho Lehtimäki,
    [Show full text]
  • Gene Expression Studies in Depression Development and Treatment
    Mariani et al. Translational Psychiatry (2021) 11:354 https://doi.org/10.1038/s41398-021-01469-6 Translational Psychiatry REVIEW ARTICLE Open Access Gene expression studies in Depression development and treatment: an overview of the underlying molecular mechanisms and biological processes to identify biomarkers Nicole Mariani 1, Nadia Cattane2,CarminePariante 1 and Annamaria Cattaneo 2,3 Abstract A combination of different risk factors, such as genetic, environmental and psychological factors, together with immune system, stress response, brain neuroplasticity and the regulation of neurotransmitters, is thought to lead to the development of major depressive disorder (MDD). A growing number of studies have tried to investigate the underlying mechanisms of MDD by analysing the expression levels of genes involved in such biological processes. These studies have shown that MDD is not just a brain disorder, but also a body disorder, and this is mainly due to the interplay between the periphery and the Central Nervous System (CNS). To this purpose, most of the studies conducted so far have mainly dedicated to the analysis of the gene expression levels using postmortem brain tissue as well as peripheral blood samples of MDD patients. In this paper, we reviewed the current literature on candidate gene expression alterations and the few existing transcriptomics studies in MDD focusing on inflammation, neuroplasticity, neurotransmitters and stress-related genes. Moreover, we focused our attention on studies, which have investigated 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; mRNA levels as biomarkers to predict therapy outcomes. This is important as many patients do not respond to antidepressant medication or could experience adverse side effects, leading to the interruption of treatment.
    [Show full text]
  • Research Article Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed Hipscs To
    Hindawi Publishing Corporation Stem Cells International Volume 2013, Article ID 784629, 25 pages http://dx.doi.org/10.1155/2013/784629 Research Article Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed hiPSCs to Differentiated Neuronal and Cardiac Progeny Leonhard Linta,1 Marianne Stockmann,1 Qiong Lin,2 André Lechel,3 Christian Proepper,1 Tobias M. Boeckers,1 Alexander Kleger,3 and Stefan Liebau1 1 InstituteforAnatomyCellBiology,UlmUniversity,Albert-EinsteinAllee11,89081Ulm,Germany 2 Institute for Biomedical Engineering, Department of Cell Biology, RWTH Aachen, Pauwelstrasse 30, 52074 Aachen, Germany 3 Department of Internal Medicine I, Ulm University, Albert-Einstein Allee 11, 89081 Ulm, Germany Correspondence should be addressed to Alexander Kleger; [email protected] and Stefan Liebau; [email protected] Received 31 January 2013; Accepted 6 March 2013 Academic Editor: Michael Levin Copyright © 2013 Leonhard Linta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Ion channels are involved in a large variety of cellular processes including stem cell differentiation. Numerous families of ion channels are present in the organism which can be distinguished by means of, for example, ion selectivity, gating mechanism, composition, or cell biological function. To characterize the distinct expression of this group of ion channels we have compared the mRNA expression levels of ion channel genes between human keratinocyte-derived induced pluripotent stem cells (hiPSCs) and their somatic cell source, keratinocytes from plucked human hair. This comparison revealed that 26% of the analyzed probes showed an upregulation of ion channels in hiPSCs while just 6% were downregulated.
    [Show full text]
  • Transcriptomic Profiling of Ca Transport Systems During
    cells Article Transcriptomic Profiling of Ca2+ Transport Systems during the Formation of the Cerebral Cortex in Mice Alexandre Bouron Genetics and Chemogenomics Lab, Université Grenoble Alpes, CNRS, CEA, INSERM, Bâtiment C3, 17 rue des Martyrs, 38054 Grenoble, France; [email protected] Received: 29 June 2020; Accepted: 24 July 2020; Published: 29 July 2020 Abstract: Cytosolic calcium (Ca2+) transients control key neural processes, including neurogenesis, migration, the polarization and growth of neurons, and the establishment and maintenance of synaptic connections. They are thus involved in the development and formation of the neural system. In this study, a publicly available whole transcriptome sequencing (RNA-Seq) dataset was used to examine the expression of genes coding for putative plasma membrane and organellar Ca2+-transporting proteins (channels, pumps, exchangers, and transporters) during the formation of the cerebral cortex in mice. Four ages were considered: embryonic days 11 (E11), 13 (E13), and 17 (E17), and post-natal day 1 (PN1). This transcriptomic profiling was also combined with live-cell Ca2+ imaging recordings to assess the presence of functional Ca2+ transport systems in E13 neurons. The most important Ca2+ routes of the cortical wall at the onset of corticogenesis (E11–E13) were TACAN, GluK5, nAChR β2, Cav3.1, Orai3, transient receptor potential cation channel subfamily M member 7 (TRPM7) non-mitochondrial Na+/Ca2+ exchanger 2 (NCX2), and the connexins CX43/CX45/CX37. Hence, transient receptor potential cation channel mucolipin subfamily member 1 (TRPML1), transmembrane protein 165 (TMEM165), and Ca2+ “leak” channels are prominent intracellular Ca2+ pathways. The Ca2+ pumps sarco/endoplasmic reticulum Ca2+ ATPase 2 (SERCA2) and plasma membrane Ca2+ ATPase 1 (PMCA1) control the resting basal Ca2+ levels.
    [Show full text]
  • Stem Cells and Ion Channels
    Stem Cells International Stem Cells and Ion Channels Guest Editors: Stefan Liebau, Alexander Kleger, Michael Levin, and Shan Ping Yu Stem Cells and Ion Channels Stem Cells International Stem Cells and Ion Channels Guest Editors: Stefan Liebau, Alexander Kleger, Michael Levin, and Shan Ping Yu Copyright © 2013 Hindawi Publishing Corporation. All rights reserved. This is a special issue published in “Stem Cells International.” All articles are open access articles distributed under the Creative Com- mons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Editorial Board Nadire N. Ali, UK Joseph Itskovitz-Eldor, Israel Pranela Rameshwar, USA Anthony Atala, USA Pavla Jendelova, Czech Republic Hannele T. Ruohola-Baker, USA Nissim Benvenisty, Israel Arne Jensen, Germany D. S. Sakaguchi, USA Kenneth Boheler, USA Sue Kimber, UK Paul R. Sanberg, USA Dominique Bonnet, UK Mark D. Kirk, USA Paul T. Sharpe, UK B. Bunnell, USA Gary E. Lyons, USA Ashok Shetty, USA Kevin D. Bunting, USA Athanasios Mantalaris, UK Igor Slukvin, USA Richard K. Burt, USA Pilar Martin-Duque, Spain Ann Steele, USA Gerald A. Colvin, USA EvaMezey,USA Alexander Storch, Germany Stephen Dalton, USA Karim Nayernia, UK Marc Turner, UK Leonard M. Eisenberg, USA K. Sue O’Shea, USA Su-Chun Zhang, USA Marina Emborg, USA J. Parent, USA Weian Zhao, USA Josef Fulka, Czech Republic Bruno Peault, USA Joel C. Glover, Norway Stefan Przyborski, UK Contents Stem Cells and Ion Channels, Stefan Liebau,
    [Show full text]
  • Ion Channels
    UC Davis UC Davis Previously Published Works Title THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels. Permalink https://escholarship.org/uc/item/1442g5hg Journal British journal of pharmacology, 176 Suppl 1(S1) ISSN 0007-1188 Authors Alexander, Stephen PH Mathie, Alistair Peters, John A et al. Publication Date 2019-12-01 DOI 10.1111/bph.14749 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: Ion channels. British Journal of Pharmacology (2019) 176, S142–S228 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels Stephen PH Alexander1 , Alistair Mathie2 ,JohnAPeters3 , Emma L Veale2 , Jörg Striessnig4 , Eamonn Kelly5, Jane F Armstrong6 , Elena Faccenda6 ,SimonDHarding6 ,AdamJPawson6 , Joanna L Sharman6 , Christopher Southan6 , Jamie A Davies6 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 3Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 4Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, A-6020 Innsbruck, Austria 5School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 6Centre for Discovery Brain Science, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties.
    [Show full text]
  • Replicated Risk Nicotinic Cholinergic Receptor Genes for Nicotine Dependence
    G C A T T A C G G C A T genes Article Replicated Risk Nicotinic Cholinergic Receptor Genes for Nicotine Dependence Lingjun Zuo 1, Rolando Garcia-Milian 2, Xiaoyun Guo 1,3,4,*, Chunlong Zhong 5,*, Yunlong Tan 6, Zhiren Wang 6, Jijun Wang 3, Xiaoping Wang 7, Longli Kang 8, Lu Lu 9,10, Xiangning Chen 11,12, Chiang-Shan R. Li 1 and Xingguang Luo 1,6,* 1 Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06510, USA; [email protected] (L.Z.); [email protected] (C.-S.R.L.) 2 Curriculum & Research Support Department, Cushing/Whitney Medical Library, Yale University School of Medicine, New Haven, CT 06510, USA; [email protected] 3 Shanghai Mental Health Center, Shanghai 200030, China; [email protected] 4 Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06510, USA 5 Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China 6 Biological Psychiatry Research Center, Beijing Huilongguan Hospital, Beijing 100096, China; [email protected] (Y.T.); [email protected] (Z.W.) 7 Department of Neurology, Shanghai First People’s Hospital, Shanghai Jiao Tong University, Shanghai 200080, China; [email protected] 8 Key Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Diseases of Tibet Autonomous Region, Xizang Minzu University School of Medicine, Xianyang, Shanxi 712082, China; [email protected] 9 Provincial Key Laboratory for Inflammation and Molecular Drug Target, Medical
    [Show full text]