Survival in a transgenic model of FALS is independent of iNOS expression [1]

Annals of Neurology

Volumn 50, Issue 2, 2001, Pages 273-

  Son, Marjatta ^a,b   Fathallah Shaykh, Hassan M ^a   Elliott, Jeffrey L ^a  

^a UNIVERSITY OF TEXAS AT DALLAS   (United States)

^b RUSH UNIVERSITY MEDICAL CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COPPER; GENE PRODUCT; NITRIC OXIDE SYNTHASE; SUPEROXIDE DISMUTASE; ZINC;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL EXPERIMENT; ANIMAL MODEL; ASTROCYTE; CONTROLLED STUDY; CORRELATION FUNCTION; DISEASE COURSE; GENE MUTATION; KNOCKOUT MOUSE; LETTER; MICROGLIA; MOUSE; NONHUMAN; PATHOPHYSIOLOGY; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN EXPRESSION; PROTEIN LOCALIZATION; SURVIVAL; TRANSGENIC MOUSE;

EID: 0034905496     PISSN: 03645134     EISSN: None     Source Type: Journal    
DOI: 10.1002/ana.1104     Document Type: Letter

References (5)

1. Motor neuron degeneration in mice that express a human Cu,Zn dismutase mutation
2. Decreased zinc affinity of amyotrophic lateral sclerosis-associated superoxide dismutase mutants leads to enhanced catalysis of tyrosine nitration by peroxynitrite
3. Administration of nitric oxide synthase inhibitors does not alter disease course of amyotrophic lateral sclerosis SOD1 mutant transgenic mice
4. Lack of involvement of neuronal nitric oxide synthase in the pathogenesis of a transgenic mouse model of familial amyotrophic lateral sclerosis
5. Inducible nitric oxide synthase upregulation in a transgenic mouse model of familial amyotrophic lateral sclerosis