Transcriptional regulation of mammalian autophagy at a glance

Author:

Füllgrabe Jens1,Ghislat Ghita1,Cho Dong-Hyung2,Rubinsztein David C.1ORCID

Affiliation:

1. Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK

2. Department of Gerontology, Graduate School of East–West Medical Science, Kyung Hee University, Yongin 17104, South Korea

Abstract

ABSTRACT Macroautophagy, hereafter referred to as autophagy, is a catabolic process that results in the lysosomal degradation of cytoplasmic contents ranging from abnormal proteins to damaged cell organelles. It is activated  under diverse conditions, including nutrient deprivation and hypoxia. During autophagy, members of the core autophagy-related (ATG) family of proteins mediate membrane rearrangements, which lead to the engulfment and degradation of cytoplasmic cargo. Recently, the nuclear regulation of autophagy, especially by transcription factors and histone modifiers, has gained increased attention. These factors are not only involved in rapid responses to autophagic stimuli, but also regulate the long-term outcome of autophagy. Now there are more than 20 transcription factors that have been shown to be linked to the autophagic process. However, their interplay and timing appear enigmatic as several have been individually shown to act as major regulators of autophagy. This Cell Science at a Glance article and the accompanying poster highlights the main cellular regulators of transcription involved in mammalian autophagy and their target genes.

Funder

FEBS Long-Term fellowship

La Ligue Contre Le Cancer

Ministry of Health & Welfare, Republic of Korea

Wellcome Trust

Publisher

The Company of Biologists

Subject

Cell Biology

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