Sources and consequences of oxidative damage from mitochondria and neurotransmitter signaling

Author:

Brennan-Minnella Angela M.1,Arron Sarah T.2,Chou Kai-ming3,Cunningham Eric4,Cleaver James E.2

Affiliation:

1. Department of Neurology; University of California, San Francisco and Veterans Affairs Medical Center; San Francisco California

2. Department of Dermatology; University of California San Francisco; 2340 Sutter Street San Francisco California

3. Department of Pharmacology and Toxicology; Indiana University School of Medicine; 635 Barnhill Drive, Room MS 552 Indianapolis Indiana

4. Torrey Pines High School; 3710 Del Mar Heights Road San Diego California 92130

Funder

National institute of Neurological Disorders and Stroke

Luke O'Brien Foundation

E.A. Dickson Emeritus Professorship of UCSF

Tumori Foundation of California Pacific Medical Center

Simon Memorial Fund of the UCSF Academic Senate Memorial Fund

National Institutes of Health grants

Department of Veterans Affairs

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Genetics(clinical),Epidemiology

Reference73 articles.

1. The tug of DNA repair;Artsimovitch;Nature,2014

2. Role of the ATPase domain of the Cockayne syndrome group B protein in UV induced apoptosis;Balajee;Oncogene,2000

3. Repair and genetic consequences of endogenous DNA base damage in mammalian cells;Barnes;Ann Rev Genet,2004

4. Cockayne syndrome group B protein regulates DNA double-strand break repair and checkpoint activation;Batenburg;Embo J,2015

5. Impact of global genome repair versus transcription-coupled repair on ultraviolet carcinogenesis in hairless mice;Berg;Cancer Res,2000

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