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Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions.
Tu PH , et al.
Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation [see comments] [published erratum appears in Science 1995 Jul 14;269(5221):149]
Gurney ME , et al.
Evidence for defective energy homeostasis in amyotrophic lateral sclerosis: benefit of a high-energy diet in a transgenic mouse model.
Dupuis L , et al.
Focal dysfunction of the proteasome: a pathogenic factor in a mouse model of amyotrophic lateral sclerosis.
Kabashi E , et al.
The superoxide dismutase1 (sod1) G93A mutation does not promote neuronal injury after focal brain ischemia and optic nerve transection in mice.
Kilic E , et al.
Up-regulation and altered distribution of lysyl oxidase in the central nervous system of mutant SOD1 transgenic mouse model of amyotrophic lateral sclerosis.
Li PA , et al.
The arachidonic acid 5-lipoxygenase inhibitor nordihydroguaiaretic acid inhibits tumor necrosis factor alpha activation of microglia and extends survival of G93A-SOD1 transgenic mice.
West M , et al.
Caspase-12 cleavage and increased oxidative stress during motoneuron degeneration in transgenic mouse model of ALS.
Wootz H , et al.
Increased expression of the glial glutamate transporter EAAT2 modulates excitotoxicity and delays the onset but not the outcome of ALS in mice.
Guo H , et al.
Dissociation between neurodegeneration and caspase-11-mediated activation of caspase-1 and caspase-3 in a mouse model of amyotrophic lateral sclerosis.
Kang SJ , et al.
Hypoxic induction of vascular endothelial growth factor is selectively impaired in mice carrying the mutant SOD1 gene.
Murakami T , et al.
Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis.
Wu AS , et al.
Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse model.
Cifuentes-Diaz C , et al.
Lumbar motoneuron fate in a mouse model of amyotrophic lateral sclerosis.
Hamson DK , et al.
Accumulation of SOD1 mutants in postnatal motoneurons does not cause motoneuron pathology or motoneuron disease.
Lino MM , et al.
Differential expression of inflammation- and apoptosis-related genes in spinal cords of a mutant SOD1 transgenic mouse model of familial amyotrophic lateral sclerosis.
Yoshihara T , et al.
Increases in cortical glutamate concentrations in transgenic amyotrophic lateral sclerosis mice are attenuated by creatine supplementation.
Andreassen OA , et al.
Leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the SOD1 G93A murine model of familial amyotrophic lateral sclerosis.
Azari MF , et al.
Recruitment of the mitochondrial-dependent apoptotic pathway in amyotrophic lateral sclerosis.
Guegan C , et al.
The prostate apoptosis response-4 protein participates in motor neuron degeneration in amyotrophic lateral sclerosis.
Pedersen WA , et al.
Age-dependent penetrance of disease in a transgenic mouse model of familial amyotrophic lateral sclerosis.
Chiu AY , et al.


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