TRIM13 regulates ER stress induced autophagy and clonogenic ability of the cells.

Article Details

Citation

Tomar D, Singh R, Singh AK, Pandya CD, Singh R

TRIM13 regulates ER stress induced autophagy and clonogenic ability of the cells.

Biochim Biophys Acta. 2012 Feb;1823(2):316-26. doi: 10.1016/j.bbamcr.2011.11.015. Epub 2011 Dec 8.

PubMed ID
22178386 [ View in PubMed
]
Abstract

Autophagy is one of the cellular adaptive processes that provide protection against many pathological conditions like infection, cancer, neurodegeneration, and aging. Recent evidences suggest that ubiquitination plays an important role in degradation of proteins or defective organelle either through proteasome or autophagy. In this study, we describe the role of TRIM13, ER resident ubiquitin E3 ligase in induction of autophagy and its role during ER stress. The ectopic expression of TRIM13 in HEK-293 cells induces autophagy. Domain mapping showed that coiled-coil (CC) domain is required for induction of autophagy. TRIM13 is stabilized during ER stress, interacts with p62/SQSTM1 and co-localizes with DFCP1. TRIM13 regulates initiation of autophagy during ER stress and decreases the clonogenic ability of the cells. This study for the first time demonstrates the role of TRIM13 in induction of autophagy which may play an important role in regulation of ER stress and may act as tumor suppressor.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
E3 ubiquitin-protein ligase TRIM13O60858Details