VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease

Mitochondria defects caused by mutant huntingtin (mtHtt) have been implicated in Huntington's disease. Here authors show that VCP binds to mtHtt on the mitochondria, and that treatment with a peptide that disrupts this interaction reduces the cellular and behavioural deficits in mouse models of...

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Main Authors: Xing Guo, XiaoYan Sun, Di Hu, Ya-Juan Wang, Hisashi Fujioka, Rajan Vyas, Sudha Chakrapani, Amit Umesh Joshi, Yu Luo, Daria Mochly-Rosen, Xin Qi
Format: Article
Language:English
Published: Nature Portfolio 2016-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms12646
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author Xing Guo
XiaoYan Sun
Di Hu
Ya-Juan Wang
Hisashi Fujioka
Rajan Vyas
Sudha Chakrapani
Amit Umesh Joshi
Yu Luo
Daria Mochly-Rosen
Xin Qi
author_facet Xing Guo
XiaoYan Sun
Di Hu
Ya-Juan Wang
Hisashi Fujioka
Rajan Vyas
Sudha Chakrapani
Amit Umesh Joshi
Yu Luo
Daria Mochly-Rosen
Xin Qi
author_sort Xing Guo
collection DOAJ
description Mitochondria defects caused by mutant huntingtin (mtHtt) have been implicated in Huntington's disease. Here authors show that VCP binds to mtHtt on the mitochondria, and that treatment with a peptide that disrupts this interaction reduces the cellular and behavioural deficits in mouse models of HD.
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spelling doaj.art-1f55ff619f9e46718fcb0202f07879be2022-12-21T23:38:59ZengNature PortfolioNature Communications2041-17232016-08-017111710.1038/ncomms12646VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s diseaseXing Guo0XiaoYan Sun1Di Hu2Ya-Juan Wang3Hisashi Fujioka4Rajan Vyas5Sudha Chakrapani6Amit Umesh Joshi7Yu Luo8Daria Mochly-Rosen9Xin Qi10Department of Physiology & Biophysics, Case Western Reserve University School of MedicineDepartment of Physiology & Biophysics, Case Western Reserve University School of MedicineDepartment of Physiology & Biophysics, Case Western Reserve University School of MedicineCenter for Proteomics and Bioinformatics, Case Western Reserve University School of MedicineDepartment of Pharmacology, Case Western Reserve University School of MedicineDepartment of Physiology & Biophysics, Case Western Reserve University School of MedicineDepartment of Physiology & Biophysics, Case Western Reserve University School of MedicineDepartment of Chemical and Systems Biology, Stanford University School of MedicineDepartment of Neurosurgery, Case Western Reserve University School of MedicineDepartment of Chemical and Systems Biology, Stanford University School of MedicineDepartment of Physiology & Biophysics, Case Western Reserve University School of MedicineMitochondria defects caused by mutant huntingtin (mtHtt) have been implicated in Huntington's disease. Here authors show that VCP binds to mtHtt on the mitochondria, and that treatment with a peptide that disrupts this interaction reduces the cellular and behavioural deficits in mouse models of HD.https://doi.org/10.1038/ncomms12646
spellingShingle Xing Guo
XiaoYan Sun
Di Hu
Ya-Juan Wang
Hisashi Fujioka
Rajan Vyas
Sudha Chakrapani
Amit Umesh Joshi
Yu Luo
Daria Mochly-Rosen
Xin Qi
VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
Nature Communications
title VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
title_full VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
title_fullStr VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
title_full_unstemmed VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
title_short VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease
title_sort vcp recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of huntington s disease
url https://doi.org/10.1038/ncomms12646
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