Mitochondrial fission and cristae disruption increase the response of cell models of Huntington's disease to apoptotic stimuli-Reference-Cited by-同舟云学术

Mitochondrial fission and cristae disruption increase the response of cell models of Huntington's disease to apoptotic stimuli

Published:2010-11-10 Issue:12 Volume:2 Page:490-503
ISSN:1757-4676
Container-title:EMBO Molecular Medicine
language:en
Short-container-title:EMBO Mol Med

Author:

Costa Veronica¹²³,Giacomello Marta³,Hudec Roman³,Lopreiato Raffaele³,Ermak Gennady⁴,Lim Dmitri³,Malorni Walter⁵,Davies Kelvin J. A.⁴,Carafoli Ernesto³,Scorrano Luca¹²³

Affiliation:

1. Department of Cell Physiology and Medicine, University of Geneva, Geneva, Switzerland

2. Dulbecco‐Telethon Institute, Rome, Italy

3. Venetian Institute of Molecular Medicine, Padova, Italy

4. Ethel Percy Andrus Gerontology Center, Davis School of Gerontology, Division of Molecular and Computational Biology, Department of Biological Sciences, College of Letters, Arts and Sciences, University of Southern California, Los Angeles, CA, USA

5. Dipartimento del Farmaco, Istituto Superiore di Sanità, Roma, Italy

Publisher

EMBO

Subject

Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/emmm.201000102

Reference64 articles.

1. FK506 prevents mitochondrial-dependent apoptotic cell death induced by 3-nitropropionic acid in rat primary cortical cultures

2. Neurochemical and histologic characterization of striatal excitotoxic lesions produced by the mitochondrial toxin 3-nitropropionic acid

3. Mitochondrial fission in apoptosis, neurodegeneration and aging

4. Dephosphorylation by calcineurin regulates translocation of Drp1 to mitochondria

5. Mitochondrial Dynamics in Disease

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