TRPA1 deficiency is protective in cuprizone-induced demyelination-A new target against oligodendrocyte apoptosis-Reference-Cited by-同舟云学术

TRPA1 deficiency is protective in cuprizone-induced demyelination-A new target against oligodendrocyte apoptosis

Published:2016-08-29 Issue:12 Volume:64 Page:2166-2180
ISSN:0894-1491
Container-title:Glia
language:en
Short-container-title:Glia

Author:

Sághy Éva¹²,Sipos Éva³,Ács Péter³,Bölcskei Kata¹²,Pohóczky Krisztina¹²,Kemény Ágnes¹⁴,Sándor Zoltán¹²,Szőke Éva¹²⁵,Sétáló György⁴⁶,Komoly Sámuel³,Pintér Erika¹²

Affiliation:

1. Department of Pharmacology and Pharmacotherapy; Faculty of Medicine, University of Pécs; Pécs Hungary

2. Szentágothai Research Center, Molecular Pharmacology Research Group, University of Pécs; Pécs Hungary

3. Department of Neurology; Faculty of Medicine, University of Pécs; Pécs Hungary

4. Department of Medical Biology; Faculty of Medicine, University of Pécs; Pécs Hungary

5. MTA-PTE Chronic Pain Research Group; Pécs Hungary

6. Signal Transduction Research Group, Szentágothai Research Center, University of Pécs; Pécs Hungary

Funder

Hungarian Grants National Brain Research Program-A

Gedeon Richter's Talentum Foundation

Publisher

Wiley

Subject

Cellular and Molecular Neuroscience,Neurology

Reference84 articles.

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3. Distribution of oligodendrocyte loss and mitochondrial toxicity in the cuprizone-induced experimental demyelination model;Acs;J Neuroimmunol,2013

4. Transient receptor potential A1 is a sensory receptor for multiple products of oxidative stress;Andersson;J Neurosci,2008

5. Absence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matter;Armstrong;J Neurosci,2002

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