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
Biochemistry | Cell Biology | Cellular and Molecular Physiology | Molecular Biology
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.
epithelial cell, fibroblast, hepatocyte, MAPK8, MAPK9, MTOR
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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
Autophagy. 2018 Jun 28. doi: 10.1080/15548627.2018.1466013. [Epub ahead of print] Link to article on publisher's site
Barutcu S, Girnius N, Vernia S, Davis RJ. (2018). Role of the MAPK/cJun NH2-Terminal Kinase signaling pathway in starvation-induced autophagy. Davis Lab Publications. https://doi.org/10.1080/15548627.2018.1466013. Retrieved from https://escholarship.umassmed.edu/davis/92