| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Maria Maddalena Lino, Corinna Schneider, Pico Caron. Accumulation of SOD1 mutants in postnatal motoneurons does not cause motoneuron pathology or motoneuron disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 22. issue 12. 2002-07-15. PMID:12077179. |
transgenic mice expressing high levels of familial amyotrophic lateral sclerosis (fals)-associated mutant superoxide dismutase 1 (sod1) under the control of a human sod1 minigene (hmg) accumulate mutant protein ubiquitously and develop motoneuron disease. |
2002-07-15 |
2023-08-12 |
mouse |
| Takekazu Ohi, Kazuko Saita, Shinji Takechi, Kazuki Nabesima, Hirofumi Tashiro, Kazutaka Shiomi, Seiichiro Sugimoto, Tomotoshi Akematsu, Tatsuo Nakayama, Toru Iwaki, Shigeru Matsukura, Kyoko Sait. Clinical features and neuropathological findings of familial amyotrophic lateral sclerosis with a His46Arg mutation in Cu/Zn superoxide dismutase. Journal of the neurological sciences. vol 197. issue 1-2. 2002-07-03. PMID:11997070. |
we examined the characteristic clinical features of one family of familial amyotrophic lateral sclerosis (fals) with a his46arg mutation in the enzyme cu/zn superoxide dismutase-1 (sod1). |
2002-07-03 |
2023-08-12 |
Not clear |
| Lawrence J Hayward, Jorge A Rodriguez, Ji W Kim, Ashutosh Tiwari, Joy J Goto, Diane E Cabelli, Joan Selverstone Valentine, Robert H Brow. Decreased metallation and activity in subsets of mutant superoxide dismutases associated with familial amyotrophic lateral sclerosis. The Journal of biological chemistry. vol 277. issue 18. 2002-07-02. PMID:11854284. |
over 90 different mutations in the gene encoding copper/zinc superoxide dismutase (sod1) cause approximately 2% of amyotrophic lateral sclerosis (als) cases by an unknown mechanism. |
2002-07-02 |
2023-08-12 |
human |
| Jorge A Rodriguez, Joan S Valentine, Daryl K Eggers, James A Roe, Ashutosh Tiwari, Robert H Brown, Lawrence J Haywar. Familial amyotrophic lateral sclerosis-associated mutations decrease the thermal stability of distinctly metallated species of human copper/zinc superoxide dismutase. The Journal of biological chemistry. vol 277. issue 18. 2002-07-02. PMID:11854285. |
we report the thermal stability of wild type (wt) and 14 different variants of human copper/zinc superoxide dismutase (sod1) associated with familial amyotrophic lateral sclerosis (fals). |
2002-07-02 |
2023-08-12 |
human |
| Jung-Joon Sung, Hyun-Jung Kim, Smi Choi-Kwon, JoungHee Lee, Manho Kim, Kwang-Woo Le. Homocysteine induces oxidative cytotoxicity in Cu,Zn-superoxide dismutase mutant motor neuronal cell. Neuroreport. vol 13. issue 4. 2002-06-24. PMID:11930144. |
mutations in human cu,zn-superoxide dismutase (sod1) cause approximately 20% of familial amyotrophic lateral sclerosis (fals) cases. |
2002-06-24 |
2023-08-12 |
human |
| M Ceroni, D Curti, D Alimont. Amyotrophic lateral sclerosis and SOD1 gene: an overview. Functional neurology. vol 16. issue 4 Suppl. 2002-06-04. PMID:11996514. |
amyotrophic lateral sclerosis and sod1 gene: an overview. |
2002-06-04 |
2023-08-12 |
Not clear |
| Svitlana Garbuzova-Davis, Alison E Willing, Melissa Milliken, Samuel Saporta, Tanya Zigova, David W Cahill, Paul R Sanber. Positive effect of transplantation of hNT neurons (NTera 2/D1 cell-line) in a model of familial amyotrophic lateral sclerosis. Experimental neurology. vol 174. issue 2. 2002-05-02. PMID:11922659. |
the aim of this study is to determine the effects of hnt neuron transplants on motor neuron function in a mouse model of familial amyotrophic lateral sclerosis (fals) in which there is a substitution of alanine for glycine at position 93 of the human sod1 gene (g93a). |
2002-05-02 |
2023-08-12 |
mouse |
| Jamuna R Subramaniam, W Ernest Lyons, Jian Liu, Thomas B Bartnikas, Jeffrey Rothstein, Donald L Price, Don W Cleveland, Jonathan D Gitlin, Philip C Won. Mutant SOD1 causes motor neuron disease independent of copper chaperone-mediated copper loading. Nature neuroscience. vol 5. issue 4. 2002-04-30. PMID:11889469. |
copper-mediated oxidative damage is proposed to play a critical role in the pathogenesis of cu/zn superoxide dismutase (sod1)-linked familial amyotrophic lateral sclerosis (fals). |
2002-04-30 |
2023-08-12 |
mouse |
| K Fukada, S Nagano, M Satoh, C Tohyama, T Nakanishi, A Shimizu, T Yanagihara, S Sakod. Stabilization of mutant Cu/Zn superoxide dismutase (SOD1) protein by coexpressed wild SOD1 protein accelerates the disease progression in familial amyotrophic lateral sclerosis mice. The European journal of neuroscience. vol 14. issue 12. 2002-04-12. PMID:11860498. |
stabilization of mutant cu/zn superoxide dismutase (sod1) protein by coexpressed wild sod1 protein accelerates the disease progression in familial amyotrophic lateral sclerosis mice. |
2002-04-12 |
2023-08-12 |
mouse |
| K Fukada, S Nagano, M Satoh, C Tohyama, T Nakanishi, A Shimizu, T Yanagihara, S Sakod. Stabilization of mutant Cu/Zn superoxide dismutase (SOD1) protein by coexpressed wild SOD1 protein accelerates the disease progression in familial amyotrophic lateral sclerosis mice. The European journal of neuroscience. vol 14. issue 12. 2002-04-12. PMID:11860498. |
transgenic mice carrying familial amyotrophic lateral sclerosis (fals)-linked mutant cu/zn superoxide dismutase (sod1) genes such as g93a (g93a-mice) and g85r (g85r-mice) genes develop limb paresis. |
2002-04-12 |
2023-08-12 |
mouse |
| C E Shaw, A al-Chalabi, N Leig. Progress in the pathogenesis of amyotrophic lateral sclerosis. Current neurology and neuroscience reports. vol 1. issue 1. 2002-04-08. PMID:11898502. |
this decade has seen the discovery of one cause for amyotrophic lateral sclerosis (als)--mutations in the copper/zinc superoxide dismutase (sod1) gene. |
2002-04-08 |
2023-08-12 |
Not clear |
| Cynthia M J Higgins, Cheolwha Jung, Hongliu Ding, Zuoshang X. Mutant Cu, Zn superoxide dismutase that causes motoneuron degeneration is present in mitochondria in the CNS. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 22. issue 6. 2002-03-27. PMID:11886899. |
mutations in cu, zn superoxide dismutase (sod1) cause a fraction of amyotrophic lateral sclerosis (als), which involves motoneuron degeneration, paralysis, and death. |
2002-03-27 |
2023-08-12 |
mouse |
| Yoshihisa Watanabe, Asao Fujiyama, Yuta Ichiba, Masahira Hattori, Tetsushi Yada, Yoshiyuki Sakaki, Toshimichi Ikemur. Chromosome-wide assessment of replication timing for human chromosomes 11q and 21q: disease-related genes in timing-switch regions. Human molecular genetics. vol 11. issue 1. 2002-03-19. PMID:11772995. |
the transition regions contained other disease-related genes including app associated with familial alzheimer's disease (ad1), sod1 associated with familial amyotrophic lateral sclerosis (als1) and pts associated with phenylketonuria. |
2002-03-19 |
2023-08-12 |
human |
| D Jaarsma, F Rognoni, W van Duijn, H W Verspaget, E D Haasdijk, J C Holsteg. CuZn superoxide dismutase (SOD1) accumulates in vacuolated mitochondria in transgenic mice expressing amyotrophic lateral sclerosis-linked SOD1 mutations. Acta neuropathologica. vol 102. issue 4. 2002-03-12. PMID:11603803. |
mutations in the sod1 gene cause a familial form of amyotrophic lateral sclerosis (fals). |
2002-03-12 |
2023-08-12 |
mouse |
| David S Howland, Jian Liu, Yijin She, Beth Goad, Nicholas J Maragakis, Benjamin Kim, Jamie Erickson, John Kulik, Lisa DeVito, George Psaltis, Louis J DeGennaro, Don W Cleveland, Jeffrey D Rothstei. Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS). Proceedings of the National Academy of Sciences of the United States of America. vol 99. issue 3. 2002-03-07. PMID:11818550. |
focal loss of the glutamate transporter eaat2 in a transgenic rat model of sod1 mutant-mediated amyotrophic lateral sclerosis (als). |
2002-03-07 |
2023-08-12 |
mouse |
| David S Howland, Jian Liu, Yijin She, Beth Goad, Nicholas J Maragakis, Benjamin Kim, Jamie Erickson, John Kulik, Lisa DeVito, George Psaltis, Louis J DeGennaro, Don W Cleveland, Jeffrey D Rothstei. Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS). Proceedings of the National Academy of Sciences of the United States of America. vol 99. issue 3. 2002-03-07. PMID:11818550. |
transgenic overexpression of cu(+2)/zn(+2) superoxide dismutase 1 (sod1) harboring an amyotrophic lateral sclerosis (als)-linked familial genetic mutation (sod1(g93a)) in a sprague-dawley rat results in als-like motor neuron disease. |
2002-03-07 |
2023-08-12 |
mouse |
| M Watanabe, M Dykes-Hoberg, V C Culotta, D L Price, P C Wong, J D Rothstei. Histological evidence of protein aggregation in mutant SOD1 transgenic mice and in amyotrophic lateral sclerosis neural tissues. Neurobiology of disease. vol 8. issue 6. 2002-02-21. PMID:11741389. |
histological evidence of protein aggregation in mutant sod1 transgenic mice and in amyotrophic lateral sclerosis neural tissues. |
2002-02-21 |
2023-08-12 |
mouse |
| M Watanabe, M Dykes-Hoberg, V C Culotta, D L Price, P C Wong, J D Rothstei. Histological evidence of protein aggregation in mutant SOD1 transgenic mice and in amyotrophic lateral sclerosis neural tissues. Neurobiology of disease. vol 8. issue 6. 2002-02-21. PMID:11741389. |
the mechanisms leading to neurodegeneration in als (amyotrophic lateral sclerosis) are not well understood, but cytosolic protein aggregates appear to be common in sporadic and familial als as well as transgenic mouse models expressing mutant cu/zn superoxide dismutase (sod1). |
2002-02-21 |
2023-08-12 |
mouse |
| M F Azari, A Galle, E C Lopes, J Kurek, S S Cheem. Leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the SOD1 G93A murine model of familial amyotrophic lateral sclerosis. Brain research. vol 922. issue 1. 2002-02-19. PMID:11730713. |
leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the sod1 g93a murine model of familial amyotrophic lateral sclerosis. |
2002-02-19 |
2023-08-12 |
mouse |
| M F Azari, A Galle, E C Lopes, J Kurek, S S Cheem. Leukemia inhibitory factor by systemic administration rescues spinal motor neurons in the SOD1 G93A murine model of familial amyotrophic lateral sclerosis. Brain research. vol 922. issue 1. 2002-02-19. PMID:11730713. |
in this study we investigated whether intense systemic lif therapy prevents the loss of lumbar motoneurons in the transgenic sod1 g93a mouse model of familial amyotrophic lateral sclerosis. |
2002-02-19 |
2023-08-12 |
mouse |