Caspases that are activated during generation of nuclear polyglutamine aggregates are necessary for DNA fragmentation but not sufficient for cell death
- 3 November 2000
- journal article
- research article
- Published by Wiley in Journal of Neuroscience Research
- Vol. 62 (4) , 547-556
- https://doi.org/10.1002/1097-4547(20001115)62:4<547::aid-jnr9>3.0.co;2-g
Abstract
No abstract availableKeywords
This publication has 50 references indexed in Scilit:
- Detection of caspase-9 activation in the cell death of the Bcl-x-deficient mouse embryo nervous system by cleavage sites-directed antiseraDevelopmental Brain Research, 2000
- Analysis of the Role of Heat Shock Protein (Hsp) Molecular Chaperones in Polyglutamine DiseaseJournal of Neuroscience, 1999
- Progress in pathogenesis studies of spinocerebellar ataxia type 1Philosophical Transactions Of The Royal Society B-Biological Sciences, 1999
- Proteases to die forGenes & Development, 1998
- Wortmannin enhances activation of CPP32 (Caspase-3) induced by TNF or anti-FasCell Death & Differentiation, 1998
- A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICADNature, 1998
- Aggregation of Huntingtin in Neuronal Intranuclear Inclusions and Dystrophic Neurites in BrainScience, 1997
- Involvement of MACH, a Novel MORT1/FADD-Interacting Protease, in Fas/APO-1- and TNF Receptor–Induced Cell DeathCell, 1996
- Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation.The Journal of cell biology, 1992
- A new technique for the assay of infectivity of human adenovirus 5 DNAVirology, 1973