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Drp1/Fis1-mediated mitochondrial fragmentation leads to lysosomal dysfunction in cardiac models of Huntington's disease.
Joshi, A U; Ebert, A E; Haileselassie, B; Mochly-Rosen, D.
Affiliation
  • Joshi AU; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, United States.
  • Ebert AE; Department of Cardiology and Pneumology, Gottingen University Medical Center, Gottingen, Germany; DZHK (German Center for Cardiovascular Research), partner site Gottingen, Germany.
  • Haileselassie B; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, United States; Department of Pediatrics division of Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, United States.
  • Mochly-Rosen D; Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, United States. Electronic address: mochly@stanford.edu.
J Mol Cell Cardiol ; 127: 125-133, 2019 02.
Article in En | MEDLINE | ID: mdl-30550751
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Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Huntington Disease / Mitochondrial Proteins / Dynamins / Lysosomes / Mitochondria Limits: Animals / Humans Language: En Journal: J Mol Cell Cardiol Year: 2019 Document type: Article
Fulltext
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PubMed Links
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Full text: 1 Collection: 01-internacional Health context: 6_ODS3_enfermedades_notrasmisibles Database: MEDLINE Main subject: Huntington Disease / Mitochondrial Proteins / Dynamins / Lysosomes / Mitochondria Limits: Animals / Humans Language: En Journal: J Mol Cell Cardiol Year: 2019 Document type: Article