Preventing mutant huntingtin proteolysis and intermittent fasting promote autophagy in models of Huntington disease-Reference-Cited by-同舟云学术

Preventing mutant huntingtin proteolysis and intermittent fasting promote autophagy in models of Huntington disease

Published:2018-03-06 Issue:1 Volume:6 Page:
ISSN:2051-5960
Container-title:Acta Neuropathologica Communications
language:en
Short-container-title:acta neuropathol commun

Author:

Ehrnhoefer Dagmar E.,Martin Dale D. O.,Schmidt Mandi E.,Qiu Xiaofan,Ladha Safia,Caron Nicholas S.,Skotte Niels H.,Nguyen Yen T. N.,Vaid Kuljeet,Southwell Amber L.,Engemann Sabine,Franciosi Sonia,Hayden Michael R.

Funder

Government of Canada

Canadian Institutes of Health Research

Michael Smith Foundation for Health Research

University of British Columbia

Teva Pharmaceutical Industries

Publisher

Springer Science and Business Media LLC

Subject

Cellular and Molecular Neuroscience,Neurology (clinical),Pathology and Forensic Medicine

Link

http://link.springer.com/content/pdf/10.1186/s40478-018-0518-0.pdf

Reference64 articles.

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4. Babu JR, Seibenhener ML, Peng J, Strom AL, Kemppainen R, Cox N, Zhu H, Wooten MC, Diaz-Meco MT, Moscat J et al (2008) Genetic inactivation of p62 leads to accumulation of hyperphosphorylated tau and neurodegeneration. J Neurochem 106:107–120. https://doi.org/10.1111/j.1471-4159.2008.05340.x

5. Bae SH, Sung SH, Oh SY, Lim JM, Lee SK, Park YN, Lee HE, Kang D, Rhee SG (2013) Sestrins activate Nrf2 by promoting p62-dependent autophagic degradation of Keap1 and prevent oxidative liver damage. Cell Metab 17:73–84. https://doi.org/10.1016/j.cmet.2012.12.002

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