Non-canonical activation of DAPK2 by AMPK constitutes a new pathway linking metabolic stress to autophagy

Ruth Shiloh; Yuval Gilad; Yaara Ber; Miriam Eisenstein; Dina Aweida; Shani Bialik; Shenhav Cohen; Adi Kimchi

doi:10.1038/s41467-018-03907-4

Nature Communications (May 2018)

Non-canonical activation of DAPK2 by AMPK constitutes a new pathway linking metabolic stress to autophagy

Ruth Shiloh,
Yuval Gilad,
Yaara Ber,
Miriam Eisenstein,
Dina Aweida,
Shani Bialik,
Shenhav Cohen,
Adi Kimchi

Affiliations

Ruth Shiloh: Department of Molecular Genetics, Weizmann Institute of Science
Yuval Gilad: Department of Molecular Genetics, Weizmann Institute of Science
Yaara Ber: Department of Molecular Genetics, Weizmann Institute of Science
Miriam Eisenstein: Department of Chemical Research Support, Weizmann Institute of Science
Dina Aweida: Faculty of Biology, Technion Israel Institute of Technology
Shani Bialik: Department of Molecular Genetics, Weizmann Institute of Science
Shenhav Cohen: Faculty of Biology, Technion Israel Institute of Technology
Adi Kimchi: Department of Molecular Genetics, Weizmann Institute of Science

DOI: https://doi.org/10.1038/s41467-018-03907-4
Journal volume & issue: Vol. 9, no. 1
pp. 1 – 15

Abstract

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DAPK2 is a calmodulin-regulated protein kinase implicated in autophagy regulation, but how physiological stress leads to its activation is yet unknown. Here, the authors show that the central metabolic sensor AMPK phosphorylates DAPK2 to promote autophagy in a calmodulin-independent mechanism.

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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