The proapoptotic BCL-2 family member BIM mediates motoneuron loss in a model of amyotrophic lateral sclerosis

Cell Death Differ. 2007 Jul;14(7):1386-9. doi: 10.1038/sj.cdd.4402166. Epub 2007 May 18.

Authors

C Hetz, P Thielen, J Fisher, P Pasinelli, R H Brown, S Korsmeyer, L Glimcher

PMID: 17510659
DOI: 10.1038/sj.cdd.4402166

No abstract available

Publication types

Letter

MeSH terms

Amyotrophic Lateral Sclerosis / metabolism*
Amyotrophic Lateral Sclerosis / pathology
Amyotrophic Lateral Sclerosis / physiopathology
Animals
Apoptosis / genetics*
Apoptosis Regulatory Proteins / genetics*
Apoptosis Regulatory Proteins / metabolism*
Bcl-2-Like Protein 11
Disease Models, Animal
Down-Regulation / genetics
Humans
In Situ Nick-End Labeling
Membrane Proteins / genetics*
Membrane Proteins / metabolism*
Mice
Mice, Knockout
Mice, Transgenic
Motor Neurons / metabolism*
Motor Neurons / pathology
Mutation / genetics
Nerve Degeneration / metabolism*
Nerve Degeneration / pathology
Nerve Degeneration / physiopathology
Proto-Oncogene Proteins / genetics*
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-bcl-2 / genetics
Proto-Oncogene Proteins c-bcl-2 / metabolism
Superoxide Dismutase / genetics
Superoxide Dismutase / metabolism
Superoxide Dismutase-1
Up-Regulation / genetics
bcl-X Protein / genetics
bcl-X Protein / metabolism

Substances

Apoptosis Regulatory Proteins
BCL2L11 protein, human
Bcl-2-Like Protein 11
Bcl2l1 protein, mouse
Bcl2l11 protein, mouse
Membrane Proteins
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2
SOD1 protein, human
bcl-X Protein
Sod1 protein, mouse
Superoxide Dismutase
Superoxide Dismutase-1