Bax and Bcl‐2 Interaction in a Transgenic Mouse Model of Familial Amyotrophic Lateral Sclerosis
Open Access
- 1 December 1999
- journal article
- research article
- Published by Wiley in Journal of Neurochemistry
- Vol. 73 (6) , 2460-2468
- https://doi.org/10.1046/j.1471-4159.1999.0732460.x
Abstract
: It has been proposed that mutations in copper/zinc‐superoxide dismutase (SOD1), the only proven cause of amyotrophic lateral sclerosis (ALS), induce the disease by a toxic property that p...Keywords
This publication has 30 references indexed in Scilit:
- Inducible Nitric Oxide Synthase Up‐Regulation in a Transgenic Mouse Model of Familial Amyotrophic Lateral SclerosisJournal of Neurochemistry, 1999
- Retinal ganglion cell loss after the period of naturally occurring cell death in bcl-2−/− miceNeuroReport, 1999
- Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosisNature Medicine, 1999
- Metabolic Dysfunction in Familial, but Not Sporadic, Amyotrophic Lateral SclerosisJournal of Neurochemistry, 1998
- Inactivation of tyrosine hydroxylase by nitration following exposure to peroxynitrite and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)Proceedings of the National Academy of Sciences, 1998
- Inhibition of ICE slows ALS in miceNature, 1997
- BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during DevelopmentNeuron, 1996
- Neuropathological changes in two lines of mice carrying a transgene for mutant human Cu,Zn SOD, and in mice overexpressing wild type human SOD: a model of familial amyotrophic lateral sclerosis (FALS)Brain Research, 1995
- Motor Neuron Degeneration in Mice that Express a Human Cu,Zn Superoxide Dismutase MutationScience, 1994
- Amyotrophic Lateral Ssclerosis and Structural Defects in Cu,Zn Superoxide DismutaseScience, 1993