The histone H4 lysine 16 acetyltransferase hMOF regulates the outcome of autophagy

Jens Füllgrabe, Melinda A. Lynch-Day, Nina Heldring, Wenbo Li, Robert B. Struijk, Qi Ma, Ola Hermanson, Michael G. Rosenfeld, Daniel J. Klionsky and Bertrand Joseph ()
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Jens Füllgrabe: Cancer Centrum Karolinska, Karolinska Institutet, Stockholm 17176, Sweden
Melinda A. Lynch-Day: Cellular and Developmental Biology and Biological Chemistry, University of Michigan, Ann Arbor
Nina Heldring: Karolinska Institutet, Stockholm 17177, Sweden
Wenbo Li: Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA
Robert B. Struijk: Cancer Centrum Karolinska, Karolinska Institutet, Stockholm 17176, Sweden
Qi Ma: Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA
Ola Hermanson: Karolinska Institutet, Stockholm 17177, Sweden
Michael G. Rosenfeld: Howard Hughes Medical Institute, School of Medicine, University of California, San Diego, La Jolla, California 92093, USA
Daniel J. Klionsky: Cellular and Developmental Biology and Biological Chemistry, University of Michigan, Ann Arbor
Bertrand Joseph: Cancer Centrum Karolinska, Karolinska Institutet, Stockholm 17176, Sweden

Nature, 2013, vol. 500, issue 7463, 468-471

Abstract: Induction of autophagy is coupled to reduction of histone H4 lysine 16 acetylation through downregulation of the histone acetyltransferase hMOF, showing that histone modifications regulate the outcome of autophagy.

Date: 2013
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DOI: 10.1038/nature12313

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