| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| J Kadekawa, H Fujimura, T Yanagihara, S Sakod. A clinicopathological study of patient with familial amyotrophic lateral sclerosis associated with a two-base pair deletion in the copper/zinc superoxide dismutase (SOD1) gene. Acta neuropathologica. vol 101. issue 4. 2001-10-25. PMID:11355314. |
a clinicopathological study of patient with familial amyotrophic lateral sclerosis associated with a two-base pair deletion in the copper/zinc superoxide dismutase (sod1) gene. |
2001-10-25 |
2023-08-12 |
Not clear |
| J M Anneser, A Gmerek, J Gerkrath, G D Borasio, R Heuman. Immunosuppressant FK506 does not exert beneficial effects in symptomatic G93A superoxide dismutase-1 transgenic mice. Neuroreport. vol 12. issue 12. 2001-10-04. PMID:11522944. |
the enzyme cu/zn-superoxide dismutase (sod1), which is mutated in a familial form of amyotrophic lateral sclerosis (als), is an endogenous regulator of cn. |
2001-10-04 |
2023-08-12 |
mouse |
| H Volkel, M Scholz, J Link, M Selzle, P Werner, R Tunnemann, G Jung, A C Ludolph, A Reute. Superoxide dismutase mutations of familial amyotrophic lateral sclerosis and the oxidative inactivation of calcineurin. FEBS letters. vol 503. issue 2-3. 2001-09-20. PMID:11513882. |
approximately 10% of all familial cases of amyotrophic lateral sclerosis (fals) are linked to mutations in the sod1 gene, which encodes the copper/zinc superoxide dismutase (cuznsod). |
2001-09-20 |
2023-08-12 |
Not clear |
| Y Watanabe, Y Adachi, K Nakashim. Japanese familial amyotrophic lateral sclerosis family with a two-base deletion in the superoxide dismutase-1 gene. Neuropathology : official journal of the Japanese Society of Neuropathology. vol 21. issue 1. 2001-09-13. PMID:11304044. |
the clinical characteristics of members of a familial amyotrophic lateral sclerosis (fals) family from oki island, whose members have a 2-bp deletion at codon 126 of cu/zn superoxide dismutase (sod1) gene, are presented here. |
2001-09-13 |
2023-08-12 |
Not clear |
| S Kato, K Nakashima, S Horiuchi, R Nagai, D W Cleveland, J Liu, A Hirano, M Takikawa, M Kato, I Nakano, S Sakoda, K Asayama, E Oham. Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation. Neuropathology : official journal of the Japanese Society of Neuropathology. vol 21. issue 1. 2001-09-13. PMID:11304045. |
formation of advanced glycation end-product-modified superoxide dismutase-1 (sod1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with sod1 gene mutation, and transgenic mice expressing human sod1 gene mutation. |
2001-09-13 |
2023-08-12 |
mouse |
| S Kato, K Nakashima, S Horiuchi, R Nagai, D W Cleveland, J Liu, A Hirano, M Takikawa, M Kato, I Nakano, S Sakoda, K Asayama, E Oham. Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation. Neuropathology : official journal of the Japanese Society of Neuropathology. vol 21. issue 1. 2001-09-13. PMID:11304045. |
neuronal lewy body-like hyaline inclusions (lbhi) and astrocytic hyaline inclusions (ast-hi) are morphological hallmarks of certain familial amyotrophic lateral sclerosis (fals) patients with superoxide dismutase-1 (sod1) gene mutations, and transgenic mice expressing the human sod1 gene mutation. |
2001-09-13 |
2023-08-12 |
mouse |
| N Shibat. Transgenic mouse model for familial amyotrophic lateral sclerosis with superoxide dismutase-1 mutation. Neuropathology : official journal of the Japanese Society of Neuropathology. vol 21. issue 1. 2001-09-13. PMID:11304046. |
familial amyotrophic lateral sclerosis (als) with mutations in the gene for superoxide dismutase-1 (sod1) is clinicopathologically reproduced by transgenic mice expressing mutant forms of sod1 detectable in familial als patients. |
2001-09-13 |
2023-08-12 |
mouse |
| M M Doroudchi, S Minotti, D A Figlewicz, H D Durha. Nitrotyrosination contributes minimally to toxicity of mutant SOD1 associated with ALS. Neuroreport. vol 12. issue 6. 2001-09-13. PMID:11338199. |
enhanced production of nitrotyrosine and subsequent protein nitration has been proposed as the mechanism by which mutant sod1 causes death of motor neurons in a familial form of amyotrophic lateral sclerosis (fals-1). |
2001-09-13 |
2023-08-12 |
human |
| M Lee, D H Hyun, B Halliwell, P Jenne. Effect of overexpression of wild-type and mutant Cu/Zn-superoxide dismutases on oxidative stress and cell death induced by hydrogen peroxide, 4-hydroxynonenal or serum deprivation: potentiation of injury by ALS-related mutant superoxide dismutases and protection by Bcl-2. Journal of neurochemistry. vol 78. issue 2. 2001-08-23. PMID:11461956. |
mutations in cu/zn-superoxide dismutase (sod1) are associated with some cases of familial amyotrophic lateral sclerosis (als). |
2001-08-23 |
2023-08-12 |
mouse |
| S Kato, M Takikawa, K Nakashima, A Hirano, D W Cleveland, H Kusaka, N Shibata, M Kato, I Nakano, E Oham. New consensus research on neuropathological aspects of familial amyotrophic lateral sclerosis with superoxide dismutase 1 (SOD1) gene mutations: inclusions containing SOD1 in neurons and astrocytes. Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. vol 1. issue 3. 2001-08-16. PMID:11464950. |
new consensus research on neuropathological aspects of familial amyotrophic lateral sclerosis with superoxide dismutase 1 (sod1) gene mutations: inclusions containing sod1 in neurons and astrocytes. |
2001-08-16 |
2023-08-12 |
mouse |
| Y Watanabe, S Kato, Y Adachi, K Nakashim. Frameshift, nonsense and non amino acid altering mutations in SOD1 in familial ALS: report of a Japanese pedigree and literature review. Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. vol 1. issue 4. 2001-08-16. PMID:11465018. |
we demonstrated the clinical characteristics of each member of a family from oki island in western japan, whose members have familial amyotrophic lateral sclerosis (fals) with a 2-base pair (bp) deletion at codon 126 of cu/zn superoxide dismutase (sod1) gene. |
2001-08-16 |
2023-08-12 |
Not clear |
| M Gaudette, M Hirano, T Siddiqu. Current status of SOD1 mutations in familial amyotrophic lateral sclerosis. Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. vol 1. issue 2. 2001-08-16. PMID:11467054. |
current status of sod1 mutations in familial amyotrophic lateral sclerosis. |
2001-08-16 |
2023-08-12 |
Not clear |
| M Gaudette, M Hirano, T Siddiqu. Current status of SOD1 mutations in familial amyotrophic lateral sclerosis. Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. vol 1. issue 2. 2001-08-16. PMID:11467054. |
twenty percent of cases of familial amyotrophic lateral sclerosis (fals) have identifiable mutations in the gene for cu, zn superoxide dismutase (sod1) located on the long arm of chromosome 21. |
2001-08-16 |
2023-08-12 |
Not clear |
| H Warita, T Hayashi, T Murakami, Y Manabe, K Ab. Oxidative damage to mitochondrial DNA in spinal motoneurons of transgenic ALS mice. Brain research. Molecular brain research. vol 89. issue 1-2. 2001-07-12. PMID:11311985. |
in order to clarify a possible role of oxidative stress in motoneuron death in amyotrophic lateral sclerosis (als), we examined a presence of 8-hydroxy-2-deoxyguanosine (8-ohdg), one of the best markers of the oxidative dna damage, in the spinal cord of transgenic mice harboring a mutant cu/zn superoxide dismutase (sod1) gene. |
2001-07-12 |
2023-08-12 |
mouse |
| S Nagano, M Satoh, H Sumi, H Fujimura, C Tohyama, T Yanagihara, S Sakod. Reduction of metallothioneins promotes the disease expression of familial amyotrophic lateral sclerosis mice in a dose-dependent manner. The European journal of neuroscience. vol 13. issue 7. 2001-06-21. PMID:11298796. |
we previously reported that abnormal copper release from mutated cu, zn-superoxide dismutase (sod1) proteins might be a common toxic gain-of-function in the pathogenesis of familial amyotrophic lateral sclerosis (fals) [ogawa et al. |
2001-06-21 |
2023-08-12 |
mouse |
| A Pramatarova, J Laganière, J Roussel, K Brisebois, G A Roulea. Neuron-specific expression of mutant superoxide dismutase 1 in transgenic mice does not lead to motor impairment. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 21. issue 10. 2001-06-21. PMID:11331366. |
mutations were identified in the cu/zn superoxide dismutase gene (sod1) in approximately 15% of patients with familial amyotrophic lateral sclerosis. |
2001-06-21 |
2023-08-12 |
mouse |
| D Gestri, C Cecchi, A Tedde, S Latorraca, A Orlacchio, E Grassi, A M Massaro, G Liguri, P H St George-Hyslop, S Sorb. Lack of SOD1 gene mutations and activity alterations in two Italian families with amyotrophic lateral sclerosis. Neuroscience letters. vol 289. issue 3. 2001-05-31. PMID:10961653. |
lack of sod1 gene mutations and activity alterations in two italian families with amyotrophic lateral sclerosis. |
2001-05-31 |
2023-08-12 |
Not clear |
| D Alimonti, A Malaspina, T E Poloni, M Ceron. Genotype-phenotype correlation in familial amyotrophic lateral sclerosis with SOD1 mutation. Functional neurology. vol 15. issue 3. 2001-05-31. PMID:11062847. |
genotype-phenotype correlation in familial amyotrophic lateral sclerosis with sod1 mutation. |
2001-05-31 |
2023-08-12 |
Not clear |
| M D Nguyen, R C Larivière, J P Julie. Deregulation of Cdk5 in a mouse model of ALS: toxicity alleviated by perikaryal neurofilament inclusions. Neuron. vol 30. issue 1. 2001-05-31. PMID:11343650. |
we report here such deregulation of cdk5 activity associated with the hyperphosphorylation of tau and neurofilament (nf) proteins in mice expressing a mutant superoxide dismutase (sod1(g37r)) linked to amyotrophic lateral sclerosis (als). |
2001-05-31 |
2023-08-12 |
mouse |
| Y Takehisa, H Ujike, H Ishizu, S Terada, T Haraguchi, Y Tanaka, T Nishinaka, K Nobukuni, Y Ihara, R Namba, T Yasuda, M Nishibori, T Hayabara, S Kurod. Familial amyotrophic lateral sclerosis with a novel Leu126Ser mutation in the copper/zinc superoxide dismutase gene showing mild clinical features and lewy body-like hyaline inclusions. Archives of neurology. vol 58. issue 5. 2001-05-31. PMID:11346368. |
mutations in the sod1 gene are responsible for approximately 25% of all familial amyotrophic lateral sclerosis (als) cases. |
2001-05-31 |
2023-08-12 |
Not clear |