| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| T L Williamson, D W Clevelan. Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons. Nature neuroscience. vol 2. issue 1. 1999-04-20. PMID:10195180. |
mutations in copper/zinc superoxide dismutase 1 (sod1), primary causes of human amyotrophic lateral sclerosis (als), provoke motor neuron death through an unidentified toxic property. |
1999-04-20 |
2023-08-12 |
human |
| P Klivenyi, R J Ferrante, R T Matthews, M B Bogdanov, A M Klein, O A Andreassen, G Mueller, M Wermer, R Kaddurah-Daouk, M F Bea. Neuroprotective effects of creatine in a transgenic animal model of amyotrophic lateral sclerosis. Nature medicine. vol 5. issue 3. 1999-04-13. PMID:10086395. |
mitochondria are particularly vulnerable to oxidative stress, and mitochondrial swelling and vacuolization are among the earliest pathologic features found in two strains of transgenic amyotrophic lateral sclerosis (als) mice with sod1 mutations. |
1999-04-13 |
2023-08-12 |
mouse |
| P Barnéoud, O Cure. Beneficial effects of lysine acetylsalicylate, a soluble salt of aspirin, on motor performance in a transgenic model of amyotrophic lateral sclerosis. Experimental neurology. vol 155. issue 2. 1999-04-07. PMID:10072299. |
we have studied the effect of lysine acetylsalicylate (las; aspegic), a soluble salt of aspirin, on motor deficits in transgenic mice expressing a human superoxide dismutase sod1 mutation (gly-93 --> ala), an animal model of familial amyotrophic lateral sclerosis (fals). |
1999-04-07 |
2023-08-12 |
mouse |
| M N Upton-Rice, M E Cudkowicz, R K Mathew, D Reif, R H Brow. Administration of nitric oxide synthase inhibitors does not alter disease course of amyotrophic lateral sclerosis SOD1 mutant transgenic mice. Annals of neurology. vol 45. issue 3. 1999-03-29. PMID:10072062. |
administration of nitric oxide synthase inhibitors does not alter disease course of amyotrophic lateral sclerosis sod1 mutant transgenic mice. |
1999-03-29 |
2023-08-12 |
mouse |
| R Liu, R K Narla, I Kurinov, B Li, F M Ucku. Increased hydroxyl radical production and apoptosis in PC12 neuron cells expressing the gain-of-function mutant G93A SOD1 gene. Radiation research. vol 151. issue 2. 1999-02-19. PMID:9952297. |
mutations of the sod1 gene (formerly known as cu,zn-sod) are frequently associated with the familial form of amyotrophic lateral sclerosis (als). |
1999-02-19 |
2023-08-12 |
Not clear |
| P Pasinelli, D R Borchelt, M K Houseweart, D W Cleveland, R H Brow. Caspase-1 is activated in neural cells and tissue with amyotrophic lateral sclerosis-associated mutations in copper-zinc superoxide dismutase. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 26. 1999-01-28. PMID:9861044. |
the mechanism by which mutations in the superoxide dismutase (sod1) gene cause motor neuron degeneration in familial amyotrophic lateral sclerosis (als) is unknown. |
1999-01-28 |
2023-08-12 |
mouse |
| A Al-Chalabi, P M Andersen, B Chioza, C Shaw, P C Sham, W Robberecht, G Matthijs, W Camu, S L Marklund, L Forsgren, G Rouleau, N G Laing, P V Hurse, T Siddique, P N Leigh, J F Powel. Recessive amyotrophic lateral sclerosis families with the D90A SOD1 mutation share a common founder: evidence for a linked protective factor. Human molecular genetics. vol 7. issue 13. 1999-01-21. PMID:9817920. |
recessive amyotrophic lateral sclerosis families with the d90a sod1 mutation share a common founder: evidence for a linked protective factor. |
1999-01-21 |
2023-08-12 |
Not clear |
| J D Rothstein, M Dykes-Hoberg, L B Corson, M Becker, D W Cleveland, D L Price, V C Culotta, P C Won. The copper chaperone CCS is abundant in neurons and astrocytes in human and rodent brain. Journal of neurochemistry. vol 72. issue 1. 1999-01-21. PMID:9886096. |
mutations of sod1 are responsible for approximately 20% of familial amyotrophic lateral sclerosis (fals). |
1999-01-21 |
2023-08-12 |
mouse |
| M E Gurney, R Liu, J S Althaus, E D Hall, D A Becke. Mutant CuZn superoxide dismutase in motor neuron disease. Journal of inherited metabolic disease. vol 21. issue 5. 1998-12-03. PMID:9728338. |
mutations of the sod1 gene encoding cuzn sod are found in patients with familial amyotrophic lateral sclerosis (fals), a progressive and fatal paralytic disease that is caused by the death of motor neurons in cortex, brainstem and spinal cord. |
1998-12-03 |
2023-08-12 |
mouse |
| R Liu, J S Althaus, B R Ellerbrock, D A Becker, M E Gurne. Enhanced oxygen radical production in a transgenic mouse model of familial amyotrophic lateral sclerosis. Annals of neurology. vol 44. issue 5. 1998-12-02. PMID:9818932. |
mutations of the sod1 gene encoding copper/zinc superoxide dismutase (cuznsod) cause an inherited form of amyotrophic lateral sclerosis. |
1998-12-02 |
2023-08-12 |
mouse |
| P K Andrus, T J Fleck, M E Gurney, E D Hal. Protein oxidative damage in a transgenic mouse model of familial amyotrophic lateral sclerosis. Journal of neurochemistry. vol 71. issue 5. 1998-11-30. PMID:9798929. |
the gly93-->ala mutation in the cu,zn superoxide dismutase (cu,zn-sod) gene (sod1) found in some familial amyotrophic lateral sclerosis (fals) patients has been shown to result in an aberrant increase in hydroxyl radical production by the mutant enzyme that may cause oxidative injury to spinal motor neurons. |
1998-11-30 |
2023-08-12 |
mouse |
| Y Boukaftane, J Khoris, B Moulard, F Salachas, V Meininger, A Malafosse, W Camu, G A Roulea. Identification of six novel SOD1 gene mutations in familial amyotrophic lateral sclerosis. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques. vol 25. issue 3. 1998-11-06. PMID:9706719. |
identification of six novel sod1 gene mutations in familial amyotrophic lateral sclerosis. |
1998-11-06 |
2023-08-12 |
Not clear |
| S Sasaki, Y Ohsawa, K Yamane, H Sakuma, N Shibata, R Nakano, K Kikugawa, T Mizutani, S Tsuji, M Iwat. Familial amyotrophic lateral sclerosis with widespread vacuolation and hyaline inclusions. Neurology. vol 51. issue 3. 1998-10-20. PMID:9748044. |
this report presents a familial amyotrophic lateral sclerosis (fals) patient with widespread vacuoles and hyaline inclusions strongly immunostained with the anti-superoxide dismutase (sod1) antibody. |
1998-10-20 |
2023-08-12 |
mouse |
| R L Casareno, D Waggoner, J D Gitli. The copper chaperone CCS directly interacts with copper/zinc superoxide dismutase. The Journal of biological chemistry. vol 273. issue 37. 1998-10-13. PMID:9726962. |
dominantly inherited mutations in the gene encoding copper/zinc superoxide dismutase (sod1) result in the fatal motor neuron disease familial amyotrophic lateral sclerosis (fals). |
1998-10-13 |
2023-08-12 |
Not clear |
| L I Bruijn, M K Houseweart, S Kato, K L Anderson, S D Anderson, E Ohama, A G Reaume, R W Scott, D W Clevelan. Aggregation and motor neuron toxicity of an ALS-linked SOD1 mutant independent from wild-type SOD1. Science (New York, N.Y.). vol 281. issue 5384. 1998-10-09. PMID:9743498. |
analysis of transgenic mice expressing familial amyotrophic lateral sclerosis (als)-linked mutations in the enzyme superoxide dismutase (sod1) have shown that motor neuron death arises from a mutant-mediated toxic property or properties. |
1998-10-09 |
2023-08-12 |
mouse |
| M M Matzuk, L Dionne, Q Guo, T R Kumar, R M Lebovit. Ovarian function in superoxide dismutase 1 and 2 knockout mice. Endocrinology. vol 139. issue 9. 1998-09-23. PMID:9724058. |
dominant mutations in sod1 are associated with amyotrophic lateral sclerosis. |
1998-09-23 |
2023-08-12 |
mouse |
| M B Bogdanov, L E Ramos, Z Xu, M F Bea. Elevated "hydroxyl radical" generation in vivo in an animal model of amyotrophic lateral sclerosis. Journal of neurochemistry. vol 71. issue 3. 1998-09-21. PMID:9721759. |
mutations in the enzyme copper/zinc superoxide dismutase-1 (sod1) are associated with familial amyotrophic lateral sclerosis (fals). |
1998-09-21 |
2023-08-12 |
mouse |
| T L Williamson, L I Bruijn, Q Zhu, K L Anderson, S D Anderson, J P Julien, D W Clevelan. Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant. Proceedings of the National Academy of Sciences of the United States of America. vol 95. issue 16. 1998-09-08. PMID:9689132. |
mutations in superoxide dismutase 1 (sod1), the only proven cause of amyotrophic lateral sclerosis (als), provoke disease through an unidentified toxic property. |
1998-09-08 |
2023-08-12 |
Not clear |
| D L Price, P C Wong, D R Borchelt, C A Pardo, G Thinakaran, A P Doan, M K Lee, L J Martin, S S Sisodi. Amyotrophic lateral sclerosis and Alzheimer disease. Lessons from model systems. Revue neurologique. vol 153. issue 8-9. 1998-08-10. PMID:9683997. |
sporadic amyotrophic lateral sclerosis (als) is an age-associated disease with cytoskeletal abnormalities and death of motor neurons; familial als (fals), an autosomal dominant disease linked to mutations in superoxide dismutase 1 (sod1), is manifested by inclusions and degeneration of motor neurons. |
1998-08-10 |
2023-08-12 |
mouse |
| N P Bajaj, S T Al-Sarraj, V Anderson, M Kibble, N Leigh, C C Mille. Cyclin-dependent kinase-5 is associated with lipofuscin in motor neurones in amyotrophic lateral sclerosis. Neuroscience letters. vol 245. issue 1. 1998-07-14. PMID:9596352. |
we have studied the distribution of cyclin dependent kinase-5 (cdk-5) within spinal cord in sporadic and two superoxide dismutase type 1 (sod1) familial cases of amyotrophic lateral sclerosis (als). |
1998-07-14 |
2023-08-12 |
Not clear |