p62 Deficiency Enhances α-Synuclein Pathology in Mice-Reference-Cited by-同舟云学术

p62 Deficiency Enhances α-Synuclein Pathology in Mice

Published:2014-11-20 Issue:5 Volume:25 Page:552-564
ISSN:1015-6305
Container-title:Brain Pathology
language:en
Short-container-title:Brain Pathology

Author:

Tanji Kunikazu¹,Odagiri Saori²,Miki Yasuo¹,Maruyama Atsushi³,Nikaido Yoshikazu⁴,Mimura Junsei³,Mori Fumiaki¹,Warabi Eiji⁵,Yanagawa Toru⁵,Ueno Shinya⁴,Itoh Ken³,Wakabayashi Koichi¹

Affiliation:

1. Department of Neuropathology; Hirosaki University Graduate School of Medicine; Hirosaki Japan

2. Department of Neuroanatomy, Cell Biology and Histology; University of Tsukuba; Tsukuba Japan

3. Department of Stress Response Science; Hirosaki University Graduate School of Medicine; Hirosaki Japan

4. Department of Neurophysiology; Hirosaki University Graduate School of Medicine; Hirosaki Japan

5. Majors of Medical Sciences; University of Tsukuba; Tsukuba Japan

Funder

JSPS KAKENHI

Priority Research Grant for Young Scientists

Hirosaki University Institutional Research Grant

Research Committee for Ataxic Disease from the Ministry of Health, Labor and Welfare, Japan

Intramural Research Grant (24-5) for Neurological and Psychiatric Disorders of NCNP

Publisher

Wiley

Subject

Clinical Neurology,Pathology and Forensic Medicine,General Neuroscience

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1111/bpa.12214/fullpdf

Reference48 articles.

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2. Depletion of 26S proteasomes in mouse brain neurons causes neurodegeneration and Lewy-like inclusions resembling human pale bodies;Bedford;J Neurosci,2008

3. Nerve cells immunoreactive for p62 in select hypothalamic and brainstem nuclei of controls and Parkinson's disease cases;Braak;J Neural Transm,2011

4. Loss of autophagy in pro-opiomelanocortin neurons perturbs axon growth and causes metabolic dysregulation;Coupe;Cell Metab,2012

5. p62/SQSTM1 differentially removes the toxic mutant androgen receptor via autophagy and inclusion formation in a spinal and bulbar muscular atrophy mouse model;Doi;J Neurosci,2013

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