Please use this identifier to cite or link to this item: https://doi.org/10.3389/fcell.2020.00299
Title: The Long and the Short of PTEN in the Regulation of Mitophagy
Authors: Wang, L. 
Lu, G. 
Shen, H.-M. 
Keywords: BNIP3
mitophagy
Parkin
PINK1
PTEN
PTEN-L
Issue Date: 2020
Publisher: Frontiers Media S.A.
Citation: Wang, L., Lu, G., Shen, H.-M. (2020). The Long and the Short of PTEN in the Regulation of Mitophagy. Frontiers in Cell and Developmental Biology 8 : 299. ScholarBank@NUS Repository. https://doi.org/10.3389/fcell.2020.00299
Rights: Attribution 4.0 International
Abstract: Mitophagy is a key mitochondrial quality control mechanism for effective and selective elimination of damaged mitochondria through the autophagy-lysosome machinery. Defective mitophagy is associated with pathogenesis of important human diseases including neurodegenerative diseases, heart failure, innate immunity, and cancer. In the past two decades, the mechanistic studies of mitophagy have made many breakthroughs with the discoveries of phosphatase and tensin homolog (PTEN)-induced kinase protein 1 (PINK1)-parkin-mediated ubiquitin (Ub)-driven pathway and BCL2/adenovirus E1B 19 kDa protein-interacting proteins 3 (BNIP3)/NIX or FUN14 domain containing 1 (FUNDC1) mitochondrial receptor-mediated pathways. Recently, several isoforms of dual phosphatase PTEN, such as PTEN-long (PTEN-L), have been identified, and some of them are implicated in the mitophagy process via their protein phosphatase activity. In this review, we aim to discuss the regulatory roles of PTEN isoforms in mitophagy. These discoveries may provide new opportunities for development of novel therapeutic strategies for mitophagy-related diseases such as neurodegenerative disorders via targeting PTEN isoforms and mitophagy. © Copyright © 2020 Wang, Lu and Shen.
Source Title: Frontiers in Cell and Developmental Biology
URI: https://scholarbank.nus.edu.sg/handle/10635/199210
ISSN: 2296-634X
DOI: 10.3389/fcell.2020.00299
Rights: Attribution 4.0 International
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