Histone H2AX deficiency causes neurobehavioral deficits and impaired redox homeostasis

Urbain Weyemi; Bindu D. Paul; Adele M. Snowman; Parthav Jailwala; Andre Nussenzweig; William M. Bonner; Solomon H. Snyder

doi:10.1038/s41467-018-03948-9

Nature Communications (Apr 2018)

Histone H2AX deficiency causes neurobehavioral deficits and impaired redox homeostasis

Urbain Weyemi,
Bindu D. Paul,
Adele M. Snowman,
Parthav Jailwala,
Andre Nussenzweig,
William M. Bonner,
Solomon H. Snyder

Affiliations

Urbain Weyemi: The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine
Bindu D. Paul: The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine
Adele M. Snowman: The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine
Parthav Jailwala: Center for Cancer Research Collaborative Bioinformatics Resource, National Cancer Institute
Andre Nussenzweig: Laboratory of Genome Integrity, National Cancer Institute, NIH
William M. Bonner: Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health
Solomon H. Snyder: The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine

DOI: https://doi.org/10.1038/s41467-018-03948-9
Journal volume & issue: Vol. 9, no. 1
pp. 1 – 10

Abstract

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H2AX is a histone variant with an essential function in DNA double-strand break repair and genome stability. Here, Weyemi and colleagues show that loss of neuronal H2AX leads to locomotor dysfunction and alteration in oxidative stress response.

Published in Nature Communications

ISSN: 2041-1723 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science
Website: https://www.nature.com/ncomms/

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