| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Mark R Cookson, Fiona M Menzies, Philip Manning, Christopher J Eggett, Denise A Figlewicz, Calum J McNeil, Pamela J Sha. Cu/Zn superoxide dismutase (SOD1) mutations associated with familial amyotrophic lateral sclerosis (ALS) affect cellular free radical release in the presence of oxidative stress. Amyotrophic lateral sclerosis and other motor neuron disorders : official publication of the World Federation of Neurology, Research Group on Motor Neuron Diseases. vol 3. issue 2. 2003-01-13. PMID:12215229. |
cu/zn superoxide dismutase (sod1) mutations associated with familial amyotrophic lateral sclerosis (als) affect cellular free radical release in the presence of oxidative stress. |
2003-01-13 |
2023-08-12 |
Not clear |
| Kimiko Ito, Tomoyuki Uchiyama, Toshio Fukutake, Kimito Arai, Toshihide Kanesaka, Takamichi Hattor. [Different clinical phenotypes of siblings with familial amyotrophic lateral sclerosis showing Cys146Arg point mutation of superoxide dismutase 1 gene]. Rinsho shinkeigaku = Clinical neurology. vol 42. issue 2. 2003-01-10. PMID:12424972. |
we reported different clinical phenotypes of siblings with familial amyotrophic lateral sclerosis (fals) showing cys146arg point mutation of superoxide dismutase 1 (sod1) gene. |
2003-01-10 |
2023-08-12 |
Not clear |
| Matthew J Parton, Wendy Broom, Peter M Andersen, Ammar Al-Chalabi, P Nigel Leigh, John F Powell, Christopher E Sha. D90A-SOD1 mediated amyotrophic lateral sclerosis: a single founder for all cases with evidence for a Cis-acting disease modifier in the recessive haplotype. Human mutation. vol 20. issue 6. 2002-12-23. PMID:12442272. |
more than 100 different heterozygous mutations in copper/zinc superoxide dismutase (sod1) have been found in patients with amyotrophic lateral sclerosis (als), a fatal neurodegenerative disease. |
2002-12-23 |
2023-08-12 |
Not clear |
| Taku Sugawara, Anders Lewén, Yvan Gasche, Fengshan Yu, Pak H Cha. Overexpression of SOD1 protects vulnerable motor neurons after spinal cord injury by attenuating mitochondrial cytochrome c release. FASEB journal : official publication of the Federation of American Societies for Experimental Biology. vol 16. issue 14. 2002-12-19. PMID:12368231. |
defective cu,zn-superoxide dismutase (sod1) is responsible for some types of amyotrophic lateral sclerosis, and ventral horn motor neurons (vmn) have been shown to die through a mitochondria-dependent apoptotic pathway after chronic exposure to high levels of reactive oxygen species (ros). |
2002-12-19 |
2023-08-12 |
rat |
| Vicky Vleminckx, Philip Van Damme, Karolien Goffin, Hans Delye, Ludo Van Den Bosch, Wim Robberech. Upregulation of HSP27 in a transgenic model of ALS. Journal of neuropathology and experimental neurology. vol 61. issue 11. 2002-12-09. PMID:12430713. |
mutations of the sod1 gene underlie 1 form of familial amyotrophic lateral sclerosis (als). |
2002-12-09 |
2023-08-12 |
mouse |
| David A Cha. Electrodiagnostic approach to the patient with suspected motor neuron disease. Neurologic clinics. vol 20. issue 2. 2002-12-04. PMID:12152446. |
the diagnosis of amyotrophic lateral sclerosis (als) per se may be challenging since there is no single diagnostic test for als (with the exception of finding a mutation in the sod1 gene). |
2002-12-04 |
2023-08-12 |
Not clear |
| Hideyuki Takeuchi, Yasushi Kobayashi, Tsuyoshi Yoshihara, Jun-ichi Niwa, Manabu Doyu, Kenzo Ohtsuka, Gen Sobu. Hsp70 and Hsp40 improve neurite outgrowth and suppress intracytoplasmic aggregate formation in cultured neuronal cells expressing mutant SOD1. Brain research. vol 949. issue 1-2. 2002-11-27. PMID:12213295. |
mutations of the superoxide dismutase 1 (sod1) gene cause familial amyotrophic lateral sclerosis (fals). |
2002-11-27 |
2023-08-12 |
Not clear |
| Krishna Puttaparthi, William L Gitomer, Uma Krishnan, Marjatta Son, Bhagya Rajendran, Jeffrey L Elliot. Disease progression in a transgenic model of familial amyotrophic lateral sclerosis is dependent on both neuronal and non-neuronal zinc binding proteins. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 22. issue 20. 2002-11-25. PMID:12388585. |
mutations in the cu/zn superoxide dismutase (sod1) gene cause one form of familial amyotrophic lateral sclerosis, a progressive disorder of motor neurons leading to weakness and death of affected individuals. |
2002-11-25 |
2023-08-12 |
mouse |
| Christelle Guégan, Miquel Vila, Peter Teismann, Caiping Chen, Brigitte Onténiente, Mingwei Li, Robert M Friedlander, Serge Przedborski, Peter Teissma. Instrumental activation of bid by caspase-1 in a transgenic mouse model of ALS. Molecular and cellular neurosciences. vol 20. issue 4. 2002-11-05. PMID:12213439. |
transgenic expression of mutant superoxide dismutase-1 (sod1) produces an animal model of amyotrophic lateral sclerosis (als), a fatal neurodegenerative disorder. |
2002-11-05 |
2023-08-12 |
mouse |
| Fiona M Menzies, Andrew J Grierson, Mark R Cookson, Paul R Heath, Janine Tomkins, Denise A Figlewicz, Paul G Ince, Pamela J Sha. Selective loss of neurofilament expression in Cu/Zn superoxide dismutase (SOD1) linked amyotrophic lateral sclerosis. Journal of neurochemistry. vol 82. issue 5. 2002-10-18. PMID:12358759. |
selective loss of neurofilament expression in cu/zn superoxide dismutase (sod1) linked amyotrophic lateral sclerosis. |
2002-10-18 |
2023-08-12 |
mouse |
| Marina Mattiazzi, Marilena D'Aurelio, Carl D Gajewski, Katherine Martushova, Mahmoud Kiaei, M Flint Beal, Giovanni Manfred. Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice. The Journal of biological chemistry. vol 277. issue 33. 2002-09-20. PMID:12050154. |
a growing body of evidence suggests that impaired mitochondrial energy production and increased oxidative radical damage to the mitochondria could be causally involved in motor neuron death in amyotrophic lateral sclerosis (als) and in familial als associated with mutations of cu,zn superoxide dismutase (sod1). |
2002-09-20 |
2023-08-12 |
mouse |
| A García-Redondo, F Bustos, B Juan Y Seva, P Del Hoyo, S Jiménez, Y Campos, M A Martín, J C Rubio, F Cañadillas, J Arenas, J Esteba. Molecular analysis of the superoxide dismutase 1 gene in Spanish patients with sporadic or familial amyotrophic lateral sclerosis. Muscle & nerve. vol 26. issue 2. 2002-09-19. PMID:12210393. |
we performed a genetic analysis of the cu/zn superoxide dismutase gene (sod1) in spanish patients with sporadic or familial amyotrophic lateral sclerosis (als). |
2002-09-19 |
2023-08-12 |
Not clear |
| Jiou Wang, Guilian Xu, Victoria Gonzales, Michael Coonfield, David Fromholt, Neal G Copeland, Nancy A Jenkins, David R Borchel. Fibrillar inclusions and motor neuron degeneration in transgenic mice expressing superoxide dismutase 1 with a disrupted copper-binding site. Neurobiology of disease. vol 10. issue 2. 2002-09-06. PMID:12127151. |
mutations in cu/zn superoxide dismutase 1 (sod1) have been linked to dominantly inherited forms of amyotrophic lateral sclerosis (fals). |
2002-09-06 |
2023-08-12 |
mouse |
| M Yamamoto, Y Kobayashi, M Li, H Niwa, N Mitsuma, Y Ito, T Muramatsu, G Sobu. In vivo gene electroporation of glial cell line-derived neurotrophic factor (GDNF) into skeletal muscle of SOD1 mutant mice. Neurochemical research. vol 26. issue 11. 2002-09-04. PMID:11874201. |
motor neurons degenerate with intracellular vacuolar change and eventually disappear in spinal cords of sod1 mutant mice, resembling human amyotrophic lateral sclerosis (als). |
2002-09-04 |
2023-08-12 |
mouse |
| Shinsuke Ishigaki, Yideng Liang, Masahiko Yamamoto, Jun-ichi Niwa, Yoshio Ando, Tsuyoshi Yoshihara, Hideyuki Takeuchi, Manabu Doyu, Gen Sobu. X-Linked inhibitor of apoptosis protein is involved in mutant SOD1-mediated neuronal degeneration. Journal of neurochemistry. vol 82. issue 3. 2002-08-30. PMID:12153481. |
mutations in the superoxide dismutase 1 (sod1) gene cause the degeneration of motor neurons in familial amyotrophic lateral sclerosis (fals). |
2002-08-30 |
2023-08-12 |
mouse |
| Fiona M Menzies, Mark R Cookson, Robert W Taylor, Douglass M Turnbull, Zofia M A Chrzanowska-Lightowlers, Lichun Dong, Denise A Figlewicz, Pamela J Sha. Mitochondrial dysfunction in a cell culture model of familial amyotrophic lateral sclerosis. Brain : a journal of neurology. vol 125. issue Pt 7. 2002-08-15. PMID:12077002. |
the molecular mechanisms by which mutations in the gene for cu/zn superoxide dismutase (sod1) lead to the selective death of motor neurones in familial amyotrophic lateral sclerosis (fals) remain incompletely understood. |
2002-08-15 |
2023-08-12 |
human |
| Fiona M Menzies, Mark R Cookson, Robert W Taylor, Douglass M Turnbull, Zofia M A Chrzanowska-Lightowlers, Lichun Dong, Denise A Figlewicz, Pamela J Sha. Mitochondrial dysfunction in a cell culture model of familial amyotrophic lateral sclerosis. Brain : a journal of neurology. vol 125. issue Pt 7. 2002-08-15. PMID:12077002. |
therapeutic measures aimed at protecting mitochondrial respiratory chain function may be useful in sod1 related familial and possibly other forms of amyotrophic lateral sclerosis. |
2002-08-15 |
2023-08-12 |
human |
| Francesco Fornai, Maria Teresa Carrì, Alberto Ferri, Egle Paolucci, Simona Prisco, Giorgio Bernardi, Giuseppe Rotilio, Nicola Biagio Mercur. Resistance to striatal dopamine depletion induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice expressing human mutant Cu,Zn superoxide dismutase. Neuroscience letters. vol 325. issue 2. 2002-08-06. PMID:12044637. |
in the present study we investigated whether a mutant form of sod1 (g93a), occurring in humans affected by amyotrophic lateral sclerosis, leads to a differential vulnerability of nigrostriatal dopaminergic neurons to the chronic dopamine depletion induced by the selective neurotoxin mptp. |
2002-08-06 |
2023-08-12 |
mouse |
| Kenneth Hensley, Robert A Floyd, Brian Gordon, Shenyun Mou, Quentin N Pye, Charles Stewart, Melinda West, Kelly Williamso. Temporal patterns of cytokine and apoptosis-related gene expression in spinal cords of the G93A-SOD1 mouse model of amyotrophic lateral sclerosis. Journal of neurochemistry. vol 82. issue 2. 2002-08-06. PMID:12124437. |
familial amyotrophic lateral sclerosis (fals) is often caused by gain-of-function mutations in cu,zn-superoxide dismutase (sod1). |
2002-08-06 |
2023-08-12 |
mouse |
| Ayako Okado-Matsumoto, Irwin Fridovic. Amyotrophic lateral sclerosis: a proposed mechanism. Proceedings of the National Academy of Sciences of the United States of America. vol 99. issue 13. 2002-07-19. PMID:12060716. |
missense mutations in cu,zn-superoxide dismutase (sod1) account for approximately 20% of familial amyotrophic lateral sclerosis (fals) through some, as yet undefined, toxic gain of function that leads to gradual death of motor neurons. |
2002-07-19 |
2023-08-12 |
Not clear |