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005     20240321220020.0
024 7 _ |a 10.4161/auto.6.7.13286
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024 7 _ |a pmid:20798600
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024 7 _ |a 1554-8627
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024 7 _ |a 1554-8635
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037 _ _ |a DZNE-2020-02441
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Geisler, Sven
|0 P:(DE-HGF)0
|b 0
245 _ _ |a The PINK1/Parkin-mediated mitophagy is compromised by PD-associated mutations.
260 _ _ |a Abingdon, Oxon
|c 2010
|b Taylor & Francis
264 _ 1 |3 online
|2 Crossref
|b Informa UK Limited
|c 2014-10-27
264 _ 1 |3 print
|2 Crossref
|b Informa UK Limited
|c 2010-10-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
|b journal
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|s 1585310136_16441
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
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520 _ _ |a Mitochondrial dysfunction is an early sign of many neurodegenerative diseases. Very recently, two Parkinson disease (PD) associated genes, PINK1 and Parkin, were shown to mediate the degradation of damaged mitochondria via selective autophagy (mitophagy). PINK1 kinase activity is needed for prompt and efficient Parkin recruitment to impaired mitochondria. PD-associated Parkin mutations interfere with the process of mitophagy at distinct steps. Here we show that whole mitochondria are turned over via macroautophagy. Moreover, disease-associated PINK1 mutations also compromise the selective degradation of depolarized mitochondria. This may be due to the decreased physical binding activity of PD-linked PINK1 mutations to Parkin. Thus, PINK1 mutations abrogate autophagy of impaired mitochondria upstream of Parkin. In addition to compromised PINK1 kinase activity, reduced binding of PINK1 to Parkin leads to failure in Parkin mitochondrial translocation, resulting in the accumulation of damaged mitochondria, which may contribute to disease pathogenesis.
536 _ _ |a 345 - Population Studies and Genetics (POF3-345)
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|c POF3-345
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a RNA, Small Interfering
|2 NLM Chemicals
650 _ 7 |a Ubiquitin-Protein Ligases
|0 EC 2.3.2.27
|2 NLM Chemicals
650 _ 7 |a parkin protein
|0 EC 2.3.2.27
|2 NLM Chemicals
650 _ 7 |a Protein Kinases
|0 EC 2.7.-
|2 NLM Chemicals
650 _ 7 |a PTEN-induced putative kinase
|0 EC 2.7.11.1
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Autophagy: genetics
|2 MeSH
650 _ 2 |a HEK293 Cells
|2 MeSH
650 _ 2 |a HeLa Cells
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mitochondria: pathology
|2 MeSH
650 _ 2 |a Mitochondria: physiology
|2 MeSH
650 _ 2 |a Mutation
|2 MeSH
650 _ 2 |a Parkinson Disease: genetics
|2 MeSH
650 _ 2 |a Parkinson Disease: pathology
|2 MeSH
650 _ 2 |a Parkinson Disease: physiopathology
|2 MeSH
650 _ 2 |a Protein Kinases: genetics
|2 MeSH
650 _ 2 |a Protein Kinases: metabolism
|2 MeSH
650 _ 2 |a RNA, Small Interfering: genetics
|2 MeSH
650 _ 2 |a RNA, Small Interfering: metabolism
|2 MeSH
650 _ 2 |a Ubiquitin-Protein Ligases: genetics
|2 MeSH
650 _ 2 |a Ubiquitin-Protein Ligases: metabolism
|2 MeSH
700 1 _ |a Holmström, Kira M
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Treis, Angela
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Skujat, Diana
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Weber, Stephanie S
|0 P:(DE-HGF)0
|b 4
700 1 _ |a Fiesel, Fabienne C
|0 P:(DE-HGF)0
|b 5
700 1 _ |a Kahle, Philipp
|0 P:(DE-2719)2810803
|b 6
|e Corresponding author
|u dzne
700 1 _ |a Springer, Wolfdieter
|0 P:(DE-HGF)0
|b 7
|e Corresponding author
773 1 8 |a 10.4161/auto.6.7.13286
|b : Informa UK Limited, 2010-10-01
|n 7
|p 871-878
|3 journal-article
|2 Crossref
|t Autophagy
|v 6
|y 2010
|x 1554-8627
773 _ _ |a 10.4161/auto.6.7.13286
|g Vol. 6, no. 7, p. 871 - 878
|0 PERI:(DE-600)2262043-6
|n 7
|q 6:7<871 - 878
|p 871-878
|t Autophagy
|v 6
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
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|b Forschungsbereich Gesundheit
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914 1 _ |y 2010
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