NRF2 Loss Accentuates Parkinsonian Pathology and Behavioral Dysfunction in Human α-Synuclein Overexpressing Mice-Reference-Cited by-同舟云学术

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NRF2 Loss Accentuates Parkinsonian Pathology and Behavioral Dysfunction in Human α-Synuclein Overexpressing Mice

Published:2021 Issue:4 Volume:12 Page:964
ISSN:2152-5250
Container-title:Aging and disease
language:en
Short-container-title:Aging and disease

Author:

Anandhan Annadurai,Nguyen Nhat,Syal Arjun,Dreher Luke A,Dodson Matthew,Zhang Donna D,Madhavan Lalitha

Publisher

Aging and Disease

Subject

Cell Biology,Neurology (clinical),Geriatrics and Gerontology,Pathology and Forensic Medicine

Link

http://www.aginganddisease.org/fileup/2152-5250/PDF/ad-0-0-0-2105150657-1.pdf

Reference60 articles.

1. Hayes JD, Dinkova-Kostova AT (2014). The Nrf2 regulatory network provides an interface between redox and intermediary metabolism. Trends Biochem Sci, 39:199-218.

2. Tebay LE, Robertson H, Durant ST, Vitale SR, Penning TM, Dinkova-Kostova AT, et al. (2015). Mechanisms of activation of the transcription factor Nrf2 by redox stressors, nutrient cues, and energy status and the pathways through which it attenuates degenerative disease. Free Radic Biol Med, 88:108-146.

3. Dodson M, de la Vega MR, Cholanians AB, Schmidlin CJ, Chapman E, Zhang DD (2019). Modulating NRF2 in Disease: Timing Is Everything. Annu Rev Pharmacol Toxicol, 59:555-575.

4. Kobayashi A, Kang MI, Okawa H, Ohtsuji M, Zenke Y, Chiba T, et al. (2004). Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2. Mol Cell Biol, 24:7130-7139.

5. Zhang DD, Lo SC, Cross JV, Templeton DJ, Hannink M (2004). Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex. Mol Cell Biol, 24:10941-10953.

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