A nuclear option that initiates autophagy

Lyndsay Murrow; Jayanta Debnath

doi:10.1016/j.molcel.2015.01.030

A nuclear option that initiates autophagy

Mol Cell. 2015 Feb 5;57(3):393-5. doi: 10.1016/j.molcel.2015.01.030.

Authors

Lyndsay Murrow¹, Jayanta Debnath²

Affiliations

¹ Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA; Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA 94143, USA.
² Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94143, USA; Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: jayanta.debnath@ucsf.edu.

PMID: 25658203
DOI: 10.1016/j.molcel.2015.01.030

Abstract

In this issue of Molecular Cell, Huang et al. (2015) describe a nuclear pool of LC3 that is deacetylated during starvation, leading to redistribution of this essential autophagy regulator to the cytoplasm, where it can initiate autophagy.

Publication types

Comment

MeSH terms

Autophagy*
Cell Nucleus / metabolism*
Humans
Lysine / metabolism*
Microtubule-Associated Proteins / metabolism*
Sirtuin 1 / metabolism*

Substances

MAP1LC3A protein, human
Microtubule-Associated Proteins
SIRT1 protein, human
Sirtuin 1
Lysine