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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis.

Mutations in the gene encoding copper/zinc superoxide dismutase enzyme produce an animal model of familial amyotrophic lateral sclerosis (FALS), a fatal disorder characterized by paralysis. Overexpression of the proto-oncogene bcl-2 delayed onset of motor neuron disease and prolonged survival in transgenic mice expressing the FALS-linked mutation in which glycine is substituted by alanine at position 93. It did not, however, alter the duration of the disease. Overexpression of bcl-2 also attenuated the magnitude of spinal cord motor neuron degeneration in the FALS-transgenic mice.[1]

References

  1. Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis. Kostic, V., Jackson-Lewis, V., de Bilbao, F., Dubois-Dauphin, M., Przedborski, S. Science (1997) [Pubmed]
 
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