Home > Publications Database > Ret rescues mitochondrial morphology and muscle degeneration of Drosophila Pink1 mutants. > print

001     137272
005     20240615120621.0
024 7 _ |a 10.1002/embj.201284290
|2 doi
024 7 _ |a pmid:24473149
|2 pmid
024 7 _ |a pmc:PMC3983680
|2 pmc
024 7 _ |a 0261-4189
|2 ISSN
024 7 _ |a 1460-2075
|2 ISSN
024 7 _ |a altmetric:2085492
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037 _ _ |a DZNE-2020-03594
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Klein, Pontus
|b 0
245 _ _ |a Ret rescues mitochondrial morphology and muscle degeneration of Drosophila Pink1 mutants.
260 _ _ |a Hoboken, NJ [u.a.]
|c 2014
|b Wiley
264 _ 1 |3 online
|2 Crossref
|b Wiley
|c 2014-01-28
264 _ 1 |3 print
|2 Crossref
|b Wiley
|c 2014-02-18
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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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 Parkinson's disease (PD)-associated Pink1 and Parkin proteins are believed to function in a common pathway controlling mitochondrial clearance and trafficking. Glial cell line-derived neurotrophic factor (GDNF) and its signaling receptor Ret are neuroprotective in toxin-based animal models of PD. However, the mechanism by which GDNF/Ret protects cells from degenerating remains unclear. We investigated whether the Drosophila homolog of Ret can rescue Pink1 and park mutant phenotypes. We report that a signaling active version of Ret (Ret(MEN₂B) rescues muscle degeneration, disintegration of mitochondria and ATP content of Pink1 mutants. Interestingly, corresponding phenotypes of park mutants were not rescued, suggesting that the phenotypes of Pink1 and park mutants have partially different origins. In human neuroblastoma cells, GDNF treatment rescues morphological defects of PINK1 knockdown, without inducing mitophagy or Parkin recruitment. GDNF also rescues bioenergetic deficits of PINK knockdown cells. Furthermore, overexpression of Ret(MEN₂B) significantly improves electron transport chain complex I function in Pink1 mutant Drosophila. These results provide a novel mechanism underlying Ret-mediated cell protection in a situation relevant for human PD.
536 _ _ |a 341 - Molecular Signaling (POF3-341)
|0 G:(DE-HGF)POF3-341
|c POF3-341
|f POF III
|x 0
542 _ _ |i 2015-09-01
|2 Crossref
|u http://doi.wiley.com/10.1002/tdm_license_1.1
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Drosophila Proteins
|2 NLM Chemicals
650 _ 7 |a Glial Cell Line-Derived Neurotrophic Factor
|2 NLM Chemicals
650 _ 7 |a Adenosine Triphosphate
|0 8L70Q75FXE
|2 NLM Chemicals
650 _ 7 |a Ubiquitin-Protein Ligases
|0 EC 2.3.2.27
|2 NLM Chemicals
650 _ 7 |a Protein Kinases
|0 EC 2.7.-
|2 NLM Chemicals
650 _ 7 |a Proto-Oncogene Proteins c-ret
|0 EC 2.7.10.1
|2 NLM Chemicals
650 _ 7 |a Ret protein, Drosophila
|0 EC 2.7.10.1
|2 NLM Chemicals
650 _ 7 |a PINK1 protein, Drosophila
|0 EC 2.7.11.1
|2 NLM Chemicals
650 _ 7 |a PTEN-induced putative kinase
|0 EC 2.7.11.1
|2 NLM Chemicals
650 _ 7 |a Protein-Serine-Threonine Kinases
|0 EC 2.7.11.1
|2 NLM Chemicals
650 _ 7 |a park protein, Drosophila
|0 EC 6.3.2.-
|2 NLM Chemicals
650 _ 7 |a Electron Transport Complex I
|0 EC 7.1.1.2
|2 NLM Chemicals
650 _ 7 |a Dopamine
|0 VTD58H1Z2X
|2 NLM Chemicals
650 _ 2 |a Adenosine Triphosphate: metabolism
|2 MeSH
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Apoptosis
|2 MeSH
650 _ 2 |a Autophagy
|2 MeSH
650 _ 2 |a Cell Line, Tumor
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Dopamine: metabolism
|2 MeSH
650 _ 2 |a Drosophila Proteins: deficiency
|2 MeSH
650 _ 2 |a Drosophila Proteins: genetics
|2 MeSH
650 _ 2 |a Drosophila Proteins: physiology
|2 MeSH
650 _ 2 |a Drosophila melanogaster: genetics
|2 MeSH
650 _ 2 |a Drosophila melanogaster: growth & development
|2 MeSH
650 _ 2 |a Electron Transport Complex I: physiology
|2 MeSH
650 _ 2 |a Genes, Lethal
|2 MeSH
650 _ 2 |a Glial Cell Line-Derived Neurotrophic Factor: pharmacology
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Mitochondria, Muscle: ultrastructure
|2 MeSH
650 _ 2 |a Muscular Atrophy: prevention & control
|2 MeSH
650 _ 2 |a Neuroblastoma: pathology
|2 MeSH
650 _ 2 |a Neurons: ultrastructure
|2 MeSH
650 _ 2 |a Oxygen Consumption
|2 MeSH
650 _ 2 |a Parkinson Disease
|2 MeSH
650 _ 2 |a Phenotype
|2 MeSH
650 _ 2 |a Protein Kinases: deficiency
|2 MeSH
650 _ 2 |a Protein Kinases: genetics
|2 MeSH
650 _ 2 |a Protein-Serine-Threonine Kinases: deficiency
|2 MeSH
650 _ 2 |a Protein-Serine-Threonine Kinases: genetics
|2 MeSH
650 _ 2 |a Protein-Serine-Threonine Kinases: physiology
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins c-ret: genetics
|2 MeSH
650 _ 2 |a Proto-Oncogene Proteins c-ret: physiology
|2 MeSH
650 _ 2 |a Pupa
|2 MeSH
650 _ 2 |a Signal Transduction: physiology
|2 MeSH
650 _ 2 |a Ubiquitin-Protein Ligases: deficiency
|2 MeSH
650 _ 2 |a Ubiquitin-Protein Ligases: genetics
|2 MeSH
700 1 _ |a Müller-Rischart, Anne Kathrin
|0 P:(DE-2719)9000425
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700 1 _ |a Motori, Elisa
|b 2
700 1 _ |a Schönbauer, Cornelia
|b 3
700 1 _ |a Schnorrer, Frank
|b 4
700 1 _ |a Winklhofer, Konstanze F
|0 P:(DE-2719)9000369
|b 5
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700 1 _ |a Klein, Rüdiger
|0 P:(DE-HGF)0
|b 6
|e Corresponding author
773 1 8 |a 10.1002/embj.201284290
|b : Wiley, 2014-01-28
|n 4
|p 341-355
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|t The EMBO Journal
|v 33
|y 2014
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773 _ _ |a 10.1002/embj.201284290
|g Vol. 33, no. 4, p. 341 - 355
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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