Transglutaminase 2 Depletion Attenuates α-Synuclein Mediated Toxicity in Mice.

Animals Brain / metabolism Disease Models, Animal GTP-Binding Proteins / genetics Mice Mice, Transgenic Parkinson Disease Protein Glutamine gamma Glutamyltransferase 2 Transglutaminases / genetics alpha-Synuclein / genetics
Parkinson disease TG2 neuroinflammation protein aggregation α-synuclein

Journal

Neuroscience
ISSN: 1873-7544
Titre abrégé: Neuroscience
Pays: United States
ID NLM: 7605074

Informations de publication

Date de publication:
10 08 2020
Historique:
received: 25 01 2020
revised: 22 05 2020
accepted: 26 05 2020
pubmed: 6 6 2020
medline: 15 5 2021
entrez: 6 6 2020
Statut: ppublish

Résumé

α-Synuclein (α-Syn) is a key pathogenic protein in α-synucleinopathies including Parkinson disease (PD) and Dementia with Lewy Bodies. The aggregation of α-Syn is believed to be deleterious and a critical step leading to neuronal dysfunction and death. One of the factors that may contribute to the initial steps of this aggregation is crosslinking through transglutaminase 2 (TG2). We previously demonstrated that overexpression of TG2 exacerbates α-Syn toxicity in mice and yeast by increasing the higher-order species of α-Syn. Herein, we investigated whether deletion of the TG2 encoding gene could mitigate the toxicity of α-Syn in vivo. Compared with α-Syn transgenic (Syn

Identifiants

DOI: 10.1016/j.neuroscience.2020.05.047 PMID: 32502569 PMC: PMC8024061
pubmed: 32502569
pii: S0306-4522(20)30349-3
doi: 10.1016/j.neuroscience.2020.05.047
pmc: PMC8024061
mid: NIHMS1683917
pii:
doi:

Substances chimiques

alpha-Synuclein 0
Protein Glutamine gamma Glutamyltransferase 2 EC 2.3.2.13
Transglutaminases EC 2.3.2.13
GTP-Binding Proteins EC 3.6.1.-

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

58-64

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS101134
Pays : United States
Organisme : NINDS NIH HHS
ID : R33 NS096032
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS095003
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS070898
Pays : United States
Organisme : NINDS NIH HHS
ID : R21 NS096032
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS073994
Pays : United States
Organisme : NCCIH NIH HHS
ID : R01 AT006868
Pays : United States

Informations de copyright

Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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Auteurs

Jie Zhang (J)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Hilary Grosso Jasutkar (H)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Run Yan (R)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Jong-Min Woo (JM)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Kang-Woo Lee (KW)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Joo-Young Im (JY)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Eunsung Junn (E)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA.

Siiri E Iismaa (SE)

Victor Chang Cardiac Research Institute, Darlinghurst, 2010, NSW, Australia; University of NSW, Kensington 2052, NSW, Australia.

M Maral Mouradian (MM)

Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ 08854, USA. Electronic address: m.mouradian@rutgers.edu.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Système nerveux › Système nerveux central › Encéphale › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › Modèles animaux de maladie humaine › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines et peptides de signalisation intracellulaire › Protéines G › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Souris transgéniques › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Maladies du système nerveux › Maladies neurodégénératives › Maladie de Parkinson › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Enzymes et coenzymes › Enzymes › Transferases › Acyltransferases › Aminoacyltransferases › Transglutaminases › Protein glutamine gamma glutamyltransferase-2 › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Enzymes et coenzymes › Enzymes › Transferases › Acyltransferases › Aminoacyltransferases › Transglutaminases › Transglutaminase 2 Depletion Attenuates...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines associées à la maladie de Parkinson › alpha-Synucléine › Transglutaminase 2 Depletion Attenuates...