Journal Article

DKFZ-2017-02083

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Mitophagy programs: mechanisms and physiological implications of mitochondrial targeting by autophagy.

Brady, A. (First author)DKFZ* ; Brady, N. (Last author)DKFZ*

2016
Birkhäuser Basel

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Please use a persistent id in citations: doi:10.1007/s00018-015-2087-8

Abstract: Mitochondria are an essential source of ATP for cellular function, but when damaged, mitochondria generate a plethora of stress signals, which lead to cellular dysfunction and eventually programmed cell death. Thus, a major component of maintaining cellular homeostasis is the recognition and removal of dysfunctional mitochondria through autophagy-mediated degradation, i.e., mitophagy. Mitophagy further constitutes a developmental program, and undergoes a high degree of crosstalk with apoptosis. Reduced mitochondrial quality control is linked to disease pathogenesis, suggesting the importance of process elucidation as a clinical target. Recent work has revealed multiple mitophagy programs that operate independently or undergo crosstalk, and require modulated autophagy receptor activities at outer membranes of mitochondria. Here, we review these mitophagy programs, focusing on pathway mechanisms which recognize and target mitochondria for sequestration by autophagosomes, as well as mechanisms controlling pathway activities. Furthermore, we provide an introduction to the currently available methods for detecting mitophagy.

Keyword(s): BNIP3 protein, human ; Membrane Proteins ; Microtubule-Associated Proteins ; Proto-Oncogene Proteins ; Ubiquitin ; Ubiquitin-Protein Ligases ; parkin protein

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Contributing Institute(s):

1. e:Bio Nachwuchsgruppe Lysosomale Systembiologie (B190)
2. Systembiologie von Zelltod-Mechanismen (B170)

Research Program(s):

1. 312 - Functional and structural genomics (POF3-312) (POF3-312)

Appears in the scientific report 2016

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Database coverage:
; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Current Contents - Life Sciences ; Ebsco Academic Search ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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