A brief overview of BNIP3L/NIX receptor‐mediated mitophagy

Mitophagy is a form of autophagy specialized to selectively remove mitochondria. Although the PINK1/Parkin pathway is the best described mitophagy of damaged mitochondria, receptor/mediated mitophagy seems to have a pivotal role in cellular development and specialization. The most studied mitophagy...

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Autores principales:	Mija Marinković, Ivana Novak
Formato:	article
Lenguaje:	EN
Publicado:	Wiley 2021
Materias:	BNIP3L/NIX mitochondria mitophagy reticulocytes Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/f4f9eea9163347ea8bed522438fda30d
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spelling	oai:doaj.org-article:f4f9eea9163347ea8bed522438fda30d2021-12-01T13:36:12ZA brief overview of BNIP3L/NIX receptor‐mediated mitophagy2211-546310.1002/2211-5463.13307https://doaj.org/article/f4f9eea9163347ea8bed522438fda30d2021-12-01T00:00:00Zhttps://doi.org/10.1002/2211-5463.13307https://doaj.org/toc/2211-5463Mitophagy is a form of autophagy specialized to selectively remove mitochondria. Although the PINK1/Parkin pathway is the best described mitophagy of damaged mitochondria, receptor/mediated mitophagy seems to have a pivotal role in cellular development and specialization. The most studied mitophagy receptor BCL2/adenovirus E1B 19‐kDa‐interacting protein 3‐like (BNIP3L/NIX) is shown to be important for the programmed removal of healthy mitochondria during terminal differentiation of erythrocytes, but its role has been proven in various cell types. Despite recent advances in our understanding of its regulation by phosphorylation and dimerization, there remain numerous questions on how BNIP3L/NIX tightly balances between cellular life and death decisions. This brief review intends to summarize ongoing dilemmas related to BNIP3L/NIX.Mija MarinkovićIvana NovakWileyarticleBNIP3L/NIXmitochondriamitophagyreticulocytesBiology (General)QH301-705.5ENFEBS Open Bio, Vol 11, Iss 12, Pp 3230-3236 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	BNIP3L/NIX mitochondria mitophagy reticulocytes Biology (General) QH301-705.5
spellingShingle	BNIP3L/NIX mitochondria mitophagy reticulocytes Biology (General) QH301-705.5 Mija Marinković Ivana Novak A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
description	Mitophagy is a form of autophagy specialized to selectively remove mitochondria. Although the PINK1/Parkin pathway is the best described mitophagy of damaged mitochondria, receptor/mediated mitophagy seems to have a pivotal role in cellular development and specialization. The most studied mitophagy receptor BCL2/adenovirus E1B 19‐kDa‐interacting protein 3‐like (BNIP3L/NIX) is shown to be important for the programmed removal of healthy mitochondria during terminal differentiation of erythrocytes, but its role has been proven in various cell types. Despite recent advances in our understanding of its regulation by phosphorylation and dimerization, there remain numerous questions on how BNIP3L/NIX tightly balances between cellular life and death decisions. This brief review intends to summarize ongoing dilemmas related to BNIP3L/NIX.
format	article
author	Mija Marinković Ivana Novak
author_facet	Mija Marinković Ivana Novak
author_sort	Mija Marinković
title	A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
title_short	A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
title_full	A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
title_fullStr	A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
title_full_unstemmed	A brief overview of BNIP3L/NIX receptor‐mediated mitophagy
title_sort	brief overview of bnip3l/nix receptor‐mediated mitophagy
publisher	Wiley
publishDate	2021
url	https://doaj.org/article/f4f9eea9163347ea8bed522438fda30d
work_keys_str_mv	AT mijamarinkovic abriefoverviewofbnip3lnixreceptormediatedmitophagy AT ivananovak abriefoverviewofbnip3lnixreceptormediatedmitophagy AT mijamarinkovic briefoverviewofbnip3lnixreceptormediatedmitophagy AT ivananovak briefoverviewofbnip3lnixreceptormediatedmitophagy
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A brief overview of BNIP3L/NIX receptor‐mediated mitophagy

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