Molecular mechanism of the MORC4 ATPase activation

Adam H. Tencer; Khan L. Cox; Gregory M. Wright; Yi Zhang; Christopher J. Petell; Brianna J. Klein; Brian D. Strahl; Joshua C. Black; Michael G. Poirier; Tatiana G. Kutateladze

doi:10.1038/s41467-020-19278-8

Nature Communications (Oct 2020)

Molecular mechanism of the MORC4 ATPase activation

Adam H. Tencer,
Khan L. Cox,
Gregory M. Wright,
Yi Zhang,
Christopher J. Petell,
Brianna J. Klein,
Brian D. Strahl,
Joshua C. Black,
Michael G. Poirier,
Tatiana G. Kutateladze

Affiliations

Adam H. Tencer: Department of Pharmacology, University of Colorado School of Medicine
Khan L. Cox: Department of Physics, Ohio State University
Gregory M. Wright: Department of Pharmacology, University of Colorado School of Medicine
Yi Zhang: Department of Pharmacology, University of Colorado School of Medicine
Christopher J. Petell: Department of Biochemistry & Biophysics, the University of North Carolina School of Medicine, and UNC Lineberger Comprehensive Cancer Center
Brianna J. Klein: Department of Pharmacology, University of Colorado School of Medicine
Brian D. Strahl: Department of Biochemistry & Biophysics, the University of North Carolina School of Medicine, and UNC Lineberger Comprehensive Cancer Center
Joshua C. Black: Department of Pharmacology, University of Colorado School of Medicine
Michael G. Poirier: Department of Physics, Ohio State University
Tatiana G. Kutateladze: Department of Pharmacology, University of Colorado School of Medicine

DOI: https://doi.org/10.1038/s41467-020-19278-8
Journal volume & issue: Vol. 11, no. 1
pp. 1 – 13

Abstract

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Human Microrchidia 4 (MORC4) ATPase has been implicated in acute and chronic pancreatitis, inflammatory disorders and cancer. Here the authors describe the structure–function relationship of MORC4 and define the molecular mechanism for MORC4 activation.

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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