Defective mitochondrial and lysosomal trafficking in chorea-acanthocytosis is independent of Src-kinase signaling-Reference-Cited by-同舟云学术

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Defective mitochondrial and lysosomal trafficking in chorea-acanthocytosis is independent of Src-kinase signaling

Published:2018-10 Issue: Volume:92 Page:137-148
ISSN:1044-7431
Container-title:Molecular and Cellular Neuroscience
language:en
Short-container-title:Molecular and Cellular Neuroscience

Author:

Glaß Hannes,Pal Arun,Reinhardt Peter,Sterneckert Jared,Wegner Florian,Storch Alexander,Hermann Andreas

Funder

Advocacy for Neuroacanthocytosis patients

Federal Ministry of Education and Research

Publisher

Elsevier BV

Subject

Cell Biology,Cellular and Molecular Neuroscience,Molecular Biology

Reference32 articles.

1. Isolation of yeast mutants defective in protein targeting to the vacuole;Bankaitis;Proc. Natl. Acad. Sci. U. S. A.,1986

2. Prion-like transmission of protein aggregates in neurodegenerative diseases;Brundin;Nat. Rev. Mol. Cell Biol.,2010

3. Neuroacanthocytosis;Danek;Curr. Opin. Neurol.,2005

4. Erythrocyte membrane changes of chorea-acanthocytosis are the result of altered Lyn kinase activity;de Franceschi;Blood,2011

5. The Vps13p-Cdc31p complex is directly required for TGN late endosome transport and TGN homotypic fusion;De;J. Cell Biol.,2017

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3. Exome sequencing of choreoacanthocytosis reveals novel mutations in VPS13A and co-mutation in modifier gene(s);Molecular Genetics and Genomics;2023-05-20

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