Home > Publications Database > Parkin: A stress-protective E3 ubiquitin ligase maintaining mitochondrial integrity > print

001     145610
005     20200925192531.0
037 _ _ |a DZNE-2020-00940
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Müller-Rischart, Anne Kathrin
|0 P:(DE-2719)9000425
|b 0
|e First author
|u dzne
111 2 _ |a 17th European Bioenergetics Conference (EBEC)
|c Freiburg
|d 2012-09-15 - 2012-09-20
|w Germany
245 _ _ |a Parkin: A stress-protective E3 ubiquitin ligase maintaining mitochondrial integrity
260 _ _ |c 2012
336 7 _ |a Abstract
|b abstract
|m abstract
|0 PUB:(DE-HGF)1
|s 1597395527_15934
|2 PUB:(DE-HGF)
336 7 _ |a Conference Paper
|0 33
|2 EndNote
336 7 _ |a INPROCEEDINGS
|2 BibTeX
336 7 _ |a conferenceObject
|2 DRIVER
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
|m journal
336 7 _ |a Output Types/Conference Abstract
|2 DataCite
336 7 _ |a OTHER
|2 ORCID
520 _ _ |a Mitochondrial dysfunction has long been implicated in the etiopathogenesis of Parkinson's disease (PD), based on the observation that mitochondrial toxins can cause parkinsonism in humans and animal models. Research into the function and dysfunction of PD-associated genes revealed that at least some of these genes interface with pathways regulating various aspects of mitochondrial biology. Mutations in the parkin gene, encoding an E3 ubiquitin ligase, are responsible for the majority of autosomal recessive parkinsonism. Our previous work revealed that parkin is a stress-inducible protein with a wide neuroprotective capacity, preventing cell death under various stress conditions. We now present evidence that the acute stress-protective activity of parkin and its capacity to induce mitophagy are mediated by two separate and independent pathways. While a functional autophagic machinery and expression of the mitochondrial kinase PINK1 is required for parkin-induced mitophagy, these components are dispensable for the anti-apoptotic activity of parkin. We identified a signaling pathway that is essential for the anti-apoptotic activity of parkin but not for induction of mitophagy. In support of this concept, parkin seems to exert adaptive effects on mitochondria depending on the severity of mitochondrial damage. Parkin prevents stress-induced cell death under moderate stress conditions with only minor mitochondrial defects. However, when mitochondria are irreversibly damaged in response to severe stress, parkin can promote their elimination via mitophagy.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
|0 G:(DE-HGF)POF3-341
|c POF3-341
|f POF III
|x 0
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
|0 G:(DE-HGF)POF3-342
|c POF3-342
|f POF III
|x 1
700 1 _ |a Tatzelt, Jörg
|0 P:(DE-2719)9000396
|b 1
|u dzne
700 1 _ |a Winklhofer, Konstanze F
|0 P:(DE-2719)9000369
|b 2
|e Last author
|u dzne
773 _ _ |0 PERI:(DE-600)2209370-9
|n Sup
|p S77 - S78
|t Biochimica et biophysica acta / Bioenergetics
|v 1817
|y 2012
|x 0005-2728
856 4 _ |u https://www.sciencedirect.com/science/article/pii/S0005272812003970
909 C O |o oai:pub.dzne.de:145610
|p VDB
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 0
|6 P:(DE-2719)9000425
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 1
|6 P:(DE-2719)9000396
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)9000369
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-341
|2 G:(DE-HGF)POF3-300
|v Molecular Signaling
|x 0
913 1 _ |a DE-HGF
|b Forschungsbereich Gesundheit
|l Erkrankungen des Nervensystems
|1 G:(DE-HGF)POF3-340
|0 G:(DE-HGF)POF3-342
|2 G:(DE-HGF)POF3-300
|v Disease Mechanisms and Model Systems
|x 1
914 1 _ |y 2012
915 _ _ |a Nationallizenz
|0 StatID:(DE-HGF)0420
|2 StatID
|d 2020-02-27
|w ger
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2020-02-27
915 _ _ |a WoS
|0 StatID:(DE-HGF)0110
|2 StatID
|b Science Citation Index
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2020-02-27
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1190
|2 StatID
|b Biological Abstracts
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2020-02-27
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b BBA-BIOENERGETICS : 2018
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2020-02-27
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0600
|2 StatID
|b Ebsco Academic Search
|d 2020-02-27
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b ASC
|d 2020-02-27
915 _ _ |a IF < 5
|0 StatID:(DE-HGF)9900
|2 StatID
|d 2020-02-27
920 1 _ |0 I:(DE-2719)5000047
|k AG Winklhofer
|l Neurobiochemistry
|x 0
920 1 _ |0 I:(DE-2719)5000053
|k Ext AG Tatzelt
|l Ext Neurobiochemistry, LMU
|x 1
980 _ _ |a abstract
980 _ _ |a VDB
980 _ _ |a journal
980 _ _ |a I:(DE-2719)5000047
980 _ _ |a I:(DE-2719)5000053
980 _ _ |a UNRESTRICTED

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21