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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...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8634856/ https://www.ncbi.nlm.nih.gov/pubmed/34597467 http://dx.doi.org/10.1002/2211-5463.13307 |
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author | Marinković, Mija Novak, Ivana |
author_facet | Marinković, Mija Novak, Ivana |
author_sort | Marinković, Mija |
collection | PubMed |
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 | Online Article Text |
id | pubmed-8634856 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86348562021-12-08 A brief overview of BNIP3L/NIX receptor‐mediated mitophagy Marinković, Mija Novak, Ivana FEBS Open Bio Reviews 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. John Wiley and Sons Inc. 2021-10-11 /pmc/articles/PMC8634856/ /pubmed/34597467 http://dx.doi.org/10.1002/2211-5463.13307 Text en © 2021 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Marinković, Mija Novak, Ivana A brief overview of BNIP3L/NIX receptor‐mediated mitophagy |
title | 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_short | A brief overview of BNIP3L/NIX receptor‐mediated mitophagy |
title_sort | brief overview of bnip3l/nix receptor‐mediated mitophagy |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8634856/ https://www.ncbi.nlm.nih.gov/pubmed/34597467 http://dx.doi.org/10.1002/2211-5463.13307 |
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