PINK1 and Parkin: team players in stress-induced mitophagy.
Identifieur interne : 000056 ( Main/Exploration ); précédent : 000055; suivant : 000057PINK1 and Parkin: team players in stress-induced mitophagy.
Auteurs : Verian Bader [Allemagne] ; Konstanze F. Winklhofer [Allemagne]Source :
- Biological chemistry [ 1437-4315 ] ; 2020.
Abstract
Mitochondria are highly vulnerable organelles based on their complex biogenesis, entailing dependence on nuclear gene expression and efficient import strategies. They are implicated in a wide spectrum of vital cellular functions, including oxidative phosphorylation, iron-sulfur cluster synthesis, regulation of calcium homeostasis, and apoptosis. Moreover, damaged mitochondria can release mitochondrial components, such as mtDNA or cardiolipin, which are sensed as danger-associated molecular patterns and trigger innate immune signaling. Thus, dysfunctional mitochondria pose a thread not only to the cellular but also to the organismal integrity. The elimination of dysfunctional and damaged mitochondria by selective autophagy, called mitophagy, is a major mechanism of mitochondrial quality control. Certain types of stress-induced mitophagy are regulated by the mitochondrial kinase PINK1 and the E3 ubiquitin ligase Parkin, which are both linked to autosomal recessive Parkinson's disease.
DOI: 10.1515/hsz-2020-0135
PubMed: 32297878
Affiliations:
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Winklhofer</name><affiliation wicri:level="1"><nlm:affiliation>Department of Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Universitätsstrasse 150, D-44801, Bochum, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, Universitätsstrasse 150, D-44801, Bochum</wicri:regionArea><wicri:noRegion>44801, Bochum</wicri:noRegion><wicri:noRegion>44801, Bochum</wicri:noRegion><wicri:noRegion>Bochum</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biological chemistry</title><idno type="eISSN">1437-4315</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondria are highly vulnerable organelles based on their complex biogenesis, entailing dependence on nuclear gene expression and efficient import strategies. They are implicated in a wide spectrum of vital cellular functions, including oxidative phosphorylation, iron-sulfur cluster synthesis, regulation of calcium homeostasis, and apoptosis. Moreover, damaged mitochondria can release mitochondrial components, such as mtDNA or cardiolipin, which are sensed as danger-associated molecular patterns and trigger innate immune signaling. Thus, dysfunctional mitochondria pose a thread not only to the cellular but also to the organismal integrity. The elimination of dysfunctional and damaged mitochondria by selective autophagy, called mitophagy, is a major mechanism of mitochondrial quality control. Certain types of stress-induced mitophagy are regulated by the mitochondrial kinase PINK1 and the E3 ubiquitin ligase Parkin, which are both linked to autosomal recessive Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">32297878</PMID><DateRevised><Year>2020</Year><Month>11</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1437-4315</ISSN><JournalIssue CitedMedium="Internet"><Volume>401</Volume><Issue>6-7</Issue><PubDate><Year>2020</Year><Month>05</Month><Day>26</Day></PubDate></JournalIssue><Title>Biological chemistry</Title><ISOAbbreviation>Biol Chem</ISOAbbreviation></Journal><ArticleTitle>PINK1 and Parkin: team players in stress-induced mitophagy.</ArticleTitle><Pagination><MedlinePgn>891-899</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1515/hsz-2020-0135</ELocationID><ELocationID EIdType="pii" ValidYN="Y">/j/bchm.2020.401.issue-6-7/hsz-2020-0135/hsz-2020-0135.xml</ELocationID><Abstract><AbstractText>Mitochondria are highly vulnerable organelles based on their complex biogenesis, entailing dependence on nuclear gene expression and efficient import strategies. They are implicated in a wide spectrum of vital cellular functions, including oxidative phosphorylation, iron-sulfur cluster synthesis, regulation of calcium homeostasis, and apoptosis. Moreover, damaged mitochondria can release mitochondrial components, such as mtDNA or cardiolipin, which are sensed as danger-associated molecular patterns and trigger innate immune signaling. Thus, dysfunctional mitochondria pose a thread not only to the cellular but also to the organismal integrity. The elimination of dysfunctional and damaged mitochondria by selective autophagy, called mitophagy, is a major mechanism of mitochondrial quality control. 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