| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| S E Browne, A C Bowling, M J Baik, M Gurney, R H Brown, M F Bea. Metabolic dysfunction in familial, but not sporadic, amyotrophic lateral sclerosis. Journal of neurochemistry. vol 71. issue 1. 1998-07-09. PMID:9648876. |
autosomal dominant familial amyotrophic lateral sclerosis (fals) is associated with mutations in the gene encoding cu/zn superoxide dismutase (sod1). |
1998-07-09 |
2023-08-12 |
mouse |
| T Canton, J Pratt, J M Stutzmann, A Imperato, A Boirea. Glutamate uptake is decreased tardively in the spinal cord of FALS mice. Neuroreport. vol 9. issue 5. 1998-07-01. PMID:9579663. |
this study examined high affinity na+-dependent uptake of glutamate in synaptosomal preparations from spinal cord in mice that express a dominant mutation of human copper/zinc superoxide dismutase (sod1) and represent an animal model of amyotrophic lateral sclerosis (als). |
1998-07-01 |
2023-08-12 |
mouse |
| T L Parkes, A J Elia, D Dickinson, A J Hilliker, J P Phillips, G L Bouliann. Extension of Drosophila lifespan by overexpression of human SOD1 in motorneurons. Nature genetics. vol 19. issue 2. 1998-07-01. PMID:9620775. |
the association between mutations in the gene encoding the oxygen radical metabolizing enzyme cuzn superoxide dismutase (sod1) and loss of motorneurons in the brain and spinal cord that occurs in the life-shortening paralytic disease, familial amyotrophic lateral sclerosis (fals; ref. |
1998-07-01 |
2023-08-12 |
human |
| M E Cudkowicz, D McKenna-Yasek, C Chen, E T Hedley-Whyte, R H Brow. Limited corticospinal tract involvement in amyotrophic lateral sclerosis subjects with the A4V mutation in the copper/zinc superoxide dismutase gene. Annals of neurology. vol 43. issue 6. 1998-06-25. PMID:9629839. |
we examined 11 subjects with inherited amyotrophic lateral sclerosis (familial amyotrophic lateral sclerosis, fals) associated with the most common copper/zinc superoxide dismutase 1 (sod1) mutation, an alanine for valine substitution in codon 4 (a4v). |
1998-06-25 |
2023-08-12 |
human |
| L B Corson, J J Strain, V C Culotta, D W Clevelan. Chaperone-facilitated copper binding is a property common to several classes of familial amyotrophic lateral sclerosis-linked superoxide dismutase mutants. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 11. 1998-06-22. PMID:9600970. |
mutations in cu, zn superoxide dismutase (sod1) cause the neurodegenerative disease familial amyotrophic lateral sclerosis from an as-yet-unidentified toxic property(ies). |
1998-06-22 |
2023-08-12 |
human |
| J Kong, Z X. Massive mitochondrial degeneration in motor neurons triggers the onset of amyotrophic lateral sclerosis in mice expressing a mutant SOD1. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 18. issue 9. 1998-05-05. PMID:9547233. |
massive mitochondrial degeneration in motor neurons triggers the onset of amyotrophic lateral sclerosis in mice expressing a mutant sod1. |
1998-05-05 |
2023-08-12 |
mouse |
| R W Orrell, S L Marklund, J S deBelleroch. Familial ALS is associated with mutations in all exons of SOD1: a novel mutation in exon 3 (Gly72Ser). Journal of the neurological sciences. vol 153. issue 1. 1998-03-05. PMID:9455977. |
mutations of the sod1 gene, which encodes the enzyme copper/zinc superoxide dismutase, are associated with familial amyotrophic lateral sclerosis (als). |
1998-03-05 |
2023-08-12 |
human |
| A Kawata, S Kato, H Hayashi, S Hira. Prominent sensory and autonomic disturbances in familial amyotrophic lateral sclerosis with a Gly93Ser mutation in the SOD1 gene. Journal of the neurological sciences. vol 153. issue 1. 1998-03-05. PMID:9455983. |
prominent sensory and autonomic disturbances in familial amyotrophic lateral sclerosis with a gly93ser mutation in the sod1 gene. |
1998-03-05 |
2023-08-12 |
Not clear |
| A Kawata, S Kato, H Hayashi, S Hira. Prominent sensory and autonomic disturbances in familial amyotrophic lateral sclerosis with a Gly93Ser mutation in the SOD1 gene. Journal of the neurological sciences. vol 153. issue 1. 1998-03-05. PMID:9455983. |
a missense mutation (gly93-->ser) was identified in exon 4 of the cu/zn superoxide dismutase (sod1) gene of a 48-year-old japanese man with familial amyotrophic lateral sclerosis (fals). |
1998-03-05 |
2023-08-12 |
Not clear |
| J Eyer, D W Cleveland, P C Wong, A C Peterso. Pathogenesis of two axonopathies does not require axonal neurofilaments. Nature. vol 391. issue 6667. 1998-03-02. PMID:9468135. |
here, in direct contrast to this hypothesis, we show that two neurodegenerative disease models in the mouse, dystonia musculorum (dt) and a superoxide dismutase 1 (sod1)-mediated form of human motor neuron disease (amyotrophic lateral sclerosis, als), progress with little or no abatement on a transgenic background in which neurofilaments are withheld from the axonal compartment. |
1998-03-02 |
2023-08-12 |
mouse |
| J Kadekawa, H Fujimura, Y Ogawa, N Hattori, M Kaido, T Nishimura, H Yoshikawa, N Shirahata, S Sakoda, T Yanagihar. A clinicopathological study of a patient with familial amyotrophic lateral sclerosis associated with a two base pair deletion in the copper/zinc superoxide dismutase (SOD1) gene. Acta neuropathologica. vol 94. issue 6. 1998-02-20. PMID:9444365. |
a clinicopathological study of a patient with familial amyotrophic lateral sclerosis associated with a two base pair deletion in the copper/zinc superoxide dismutase (sod1) gene. |
1998-02-20 |
2023-08-12 |
Not clear |
| J Kadekawa, H Fujimura, Y Ogawa, N Hattori, M Kaido, T Nishimura, H Yoshikawa, N Shirahata, S Sakoda, T Yanagihar. A clinicopathological study of a patient with familial amyotrophic lateral sclerosis associated with a two base pair deletion in the copper/zinc superoxide dismutase (SOD1) gene. Acta neuropathologica. vol 94. issue 6. 1998-02-20. PMID:9444365. |
the recognition of mutations in the copper/zinc superoxide dismutase (sod1) gene in familial amyotrophic lateral sclerosis (fals) has been a landmark in als research. |
1998-02-20 |
2023-08-12 |
Not clear |
| M E Gurne. The use of transgenic mouse models of amyotrophic lateral sclerosis in preclinical drug studies. Journal of the neurological sciences. vol 152 Suppl 1. 1998-02-04. PMID:9419057. |
the discovery of mutations in the human sod1 gene encoding cu,zn superoxide dismutase (cu,zn sod) in patients with familial amyotrophic lateral sclerosis (als) has made possible the development of etiological models of the disease. |
1998-02-04 |
2023-08-12 |
mouse |
| B Zhang, P Tu, F Abtahian, J Q Trojanowski, V M Le. Neurofilaments and orthograde transport are reduced in ventral root axons of transgenic mice that express human SOD1 with a G93A mutation. The Journal of cell biology. vol 139. issue 5. 1997-12-30. PMID:9382875. |
mice engineered to express a transgene encoding a human cu/zn superoxide dismutase (sod1) with a gly93 --> ala (g93a) mutation found in patients who succumb to familial amyotrophic lateral sclerosis (fals) develop a rapidly progressive and fatal motor neuron disease (mnd) similar to amyotrophic lateral sclerosis (als). |
1997-12-30 |
2023-08-12 |
mouse |
| R J Ferrante, S E Browne, L A Shinobu, A C Bowling, M J Baik, U MacGarvey, N W Kowall, R H Brown, M F Bea. Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis. Journal of neurochemistry. vol 69. issue 5. 1997-11-20. PMID:9349552. |
some cases of autosomal dominant familial amyotrophic lateral sclerosis (fals) are associated with mutations in the gene encoding cu/zn superoxide dismutase (sod1), suggesting that oxidative damage may play a role in als pathogenesis. |
1997-11-20 |
2023-08-12 |
human |
| V C Culotta, L W Klomp, J Strain, R L Casareno, B Krems, J D Gitli. The copper chaperone for superoxide dismutase. The Journal of biological chemistry. vol 272. issue 38. 1997-10-23. PMID:9295278. |
elucidation of the ccs copper delivery pathway may permit development of novel therapeutic approaches to human diseases that involve sod1, including amyotrophic lateral sclerosis. |
1997-10-23 |
2023-08-12 |
human |
| R J Ferrante, L A Shinobu, J B Schulz, R T Matthews, C E Thomas, N W Kowall, M E Gurney, M F Bea. Increased 3-nitrotyrosine and oxidative damage in mice with a human copper/zinc superoxide dismutase mutation. Annals of neurology. vol 42. issue 3. 1997-10-16. PMID:9307254. |
mutations in copper/zinc superoxide dismutase (sod1) cause a subset of cases of autosomal dominant familial amyotrophic lateral sclerosis (fals). |
1997-10-16 |
2023-08-12 |
mouse |
| A F Hottinger, E G Fine, M E Gurney, A D Zurn, P Aebische. The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. The European journal of neuroscience. vol 9. issue 7. 1997-09-25. PMID:9240414. |
a subpopulation of familial cases of amyotrophic lateral sclerosis has been linked to mutations in the gene encoding cu/zn superoxide dismutase (sod1). |
1997-09-25 |
2023-08-12 |
mouse |
| A F Hottinger, E G Fine, M E Gurney, A D Zurn, P Aebische. The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. The European journal of neuroscience. vol 9. issue 7. 1997-09-25. PMID:9240414. |
to test this hypothesis in vivo, we administered the copper chelator d-penicillamine to a transgenic mouse model of familial amyotrophic lateral sclerosis overexpressing a mutated form of human sod1. |
1997-09-25 |
2023-08-12 |
mouse |
| A F Hottinger, E G Fine, M E Gurney, A D Zurn, P Aebische. The copper chelator d-penicillamine delays onset of disease and extends survival in a transgenic mouse model of familial amyotrophic lateral sclerosis. The European journal of neuroscience. vol 9. issue 7. 1997-09-25. PMID:9240414. |
these results suggest that copper chelators may benefit patients with familial amyotrophic lateral sclerosis linked to mutations in the sod1 gene. |
1997-09-25 |
2023-08-12 |
mouse |