UMMS Affiliation

Program in Molecular Medicine; Davis Lab; UMass Metabolic Network; Graduate School of Biomedical Sciences, Cancer Biology Program; Graduate School of Biomedical Sciences, Interdisciplinary Graduate Program

Publication Date

2018-06-28

Document Type

Article Postprint

Disciplines

Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology

Abstract

Autophagy is required for cellular homeostasis and can determine cell viability in response to stress. It is established that MTOR is a master regulator of starvation-induced macroautophagy/autophagy, but recent studies have also implicated an essential role for the MAPK8/cJun NH2-terminal kinase 1 signal transduction pathway. We found that MAPK8/JNK1 and MAPK9/JNK2 were not required for autophagy caused by starvation or MTOR inhibition in murine fibroblasts and epithelial cells. These data demonstrate that MAPK8/9 has no required role in starvation-induced autophagy. We conclude that the role of MAPK8/9 in autophagy may be context-dependent and more complex than previously considered.

Keywords

epithelial cell, fibroblast, hepatocyte, MAPK8, MAPK9, MTOR

Rights and Permissions

Accepted author version. This is an Open Access article. Non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly attributed, cited, and is not altered, transformed, or built upon in any way, is permitted. The moral rights of the named author(s) have been asserted.

DOI of Published Version

10.1080/15548627.2018.1466013

Source

Autophagy. 2018 Jun 28. doi: 10.1080/15548627.2018.1466013. [Epub ahead of print] Link to article on publisher's site

Journal/Book/Conference Title

Autophagy

Related Resources

Link to article in PubMed

PubMed ID

29950132

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