All Relations between Amyotrophic Lateral Sclerosis and sod1

Publication Sentence Publish Date Extraction Date Species
M Said Ahmed, W Y Hung, J S Zu, P Hockberger, T Siddiqu. Increased reactive oxygen species in familial amyotrophic lateral sclerosis with mutations in SOD1. Journal of the neurological sciences. vol 176. issue 2. 2000-10-04. PMID:10930589. increased reactive oxygen species in familial amyotrophic lateral sclerosis with mutations in sod1. 2000-10-04 2023-08-12 Not clear
C Kuntz, Y Kinoshita, M F Beal, L A Donehower, R S Morriso. Absence of p53: no effect in a transgenic mouse model of familial amyotrophic lateral sclerosis. Experimental neurology. vol 165. issue 1. 2000-10-04. PMID:10964497. familial amyotrophic lateral sclerosis (als) has been linked in some families to dominantly inherited mutations in the gene encoding copper-zinc superoxide dismutase 1 (cu-zn sod1). 2000-10-04 2023-08-12 mouse
R Mariotti, M Bentivogli. Activation and response to axotomy of microglia in the facial motor nuclei of G93A superoxide dismutase transgenic mice. Neuroscience letters. vol 285. issue 2. 2000-08-23. PMID:10793233. mice over-expressing a human mutation of cu(2+)/zn(2+) superoxide dismutase (sod1) provide a model of amyotrophic lateral sclerosis. 2000-08-23 2023-08-12 mouse
W G Johnso. Late-onset neurodegenerative diseases--the role of protein insolubility. Journal of anatomy. vol 196 ( Pt 4). 2000-08-22. PMID:10923991. in familial amyotrophic lateral sclerosis, a group of dominantly inherited disorders, sod1 precipitates are found. 2000-08-22 2023-08-12 Not clear
M Weber, A Eisen, H G Stewart, P M Anderse. Preserved slow conducting corticomotoneuronal projections in amyotrophic lateral sclerosis with autosomal recessive D90A CuZn-superoxide dismutase mutation. Brain : a journal of neurology. vol 123 ( Pt 7). 2000-08-07. PMID:10869061. recently, a subgroup of the amyotrophic lateral sclerosis (als) syndrome associated with mutations in the gene encoding the free radical scavenging enzyme cuzn-superoxide dismutase (cuzn-sod, sod1) has been identified. 2000-08-07 2023-08-12 human
N Ende, F Weinstein, R Chen, M End. Human umbilical cord blood effect on sod mice (amyotrophic lateral sclerosis). Life sciences. vol 67. issue 1. 2000-07-28. PMID:10896029. this study attempted to determine the effect of hucb on sod1 mice (transgenic b6sjl-tgn(sod1-g93a)1gur), which have a mutation of the human transgene, (cuzn superoxide dismutase gene sod1) that has been associated with amyotrophic lateral sclerosis. 2000-07-28 2023-08-12 mouse
Y Fujita, K Okamoto, A Sakurai, N K Gonatas, A Hiran. Fragmentation of the Golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with SOD1 mutations and posterior column involvement. Journal of the neurological sciences. vol 174. issue 2. 2000-06-12. PMID:10727699. fragmentation of the golgi apparatus of the anterior horn cells in patients with familial amyotrophic lateral sclerosis with sod1 mutations and posterior column involvement. 2000-06-12 2023-08-12 mouse
H Zhang, J Joseph, C Felix, B Kalyanarama. Bicarbonate enhances the hydroxylation, nitration, and peroxidation reactions catalyzed by copper, zinc superoxide dismutase. Intermediacy of carbonate anion radical. The Journal of biological chemistry. vol 275. issue 19. 2000-06-08. PMID:10799477. this new and different perspective on hco(3)(-)-mediated oxidative reactions of sod1 may help us understand the free radical mechanism of sod1 and related mutants linked to amyotrophic lateral sclerosis. 2000-06-08 2023-08-12 Not clear
M Azzouz, A Hottinger, J C Paterna, A D Zurn, P Aebischer, H Büele. Increased motoneuron survival and improved neuromuscular function in transgenic ALS mice after intraspinal injection of an adeno-associated virus encoding Bcl-2. Human molecular genetics. vol 9. issue 5. 2000-06-01. PMID:10749988. mutations in the gene encoding cu/zn superoxide dismutase (sod1) underlie some familial cases of amyotrophic lateral sclerosis (als), a neurodegenerative disorder characterized by loss of cortical, brainstem and spinal motoneurons. 2000-06-01 2023-08-12 mouse
O A Andreassen, R J Ferrante, P Klivenyi, A M Klein, L A Shinobu, C J Epstein, M F Bea. Partial deficiency of manganese superoxide dismutase exacerbates a transgenic mouse model of amyotrophic lateral sclerosis. Annals of neurology. vol 47. issue 4. 2000-04-21. PMID:10762155. the pathogenesis of neuronal cell death as a consequence of mutations in copper/zinc superoxide dismutase (sod1) associated with familial amyotrophic lateral sclerosis may involve oxidative damage and mitochondrial dysfunction. 2000-04-21 2023-08-12 mouse
M Li, V O Ona, C Guégan, M Chen, V Jackson-Lewis, L J Andrews, A J Olszewski, P E Stieg, J P Lee, S Przedborski, R M Friedlande. Functional role of caspase-1 and caspase-3 in an ALS transgenic mouse model. Science (New York, N.Y.). vol 288. issue 5464. 2000-04-20. PMID:10764647. mutations in the copper/zinc superoxide dismutase (sod1) gene produce an animal model of familial amyotrophic lateral sclerosis (als), a fatal neurodegenerative disorder. 2000-04-20 2023-08-12 mouse
Y H Gong, J L Elliot. Metallothionein expression is altered in a transgenic murine model of familial amyotrophic lateral sclerosis. Experimental neurology. vol 162. issue 1. 2000-04-18. PMID:10716886. missense mutations in the gene encoding copper zinc superoxide dismutase (sod1) have been found to cause one form of familial amyotrophic lateral sclerosis (fals). 2000-04-18 2023-08-12 mouse
B Lutz-Bucher, J L González de Aguilar, F René, V Sée, J W Gordon, J Loeffle. Oxidative stress and a murine superoxide dismutase-1 mutation promoting amyotrophic lateral sclerosis alter neurosecretion in the hypothalamo-neurohypophyseal axis. Neuroendocrinology. vol 69. issue 5. 2000-04-13. PMID:10343179. to test whether such a mechanism may operate under pathological conditions with pronounced oxidative stress, we compared neurosecretion in wild-type and transgenic mice carrying a mutated form of sod1 associated with human familial amyotrophic lateral sclerosis. 2000-04-13 2023-08-12 mouse
A Stieber, J O Gonatas, N K Gonata. Aggregation of ubiquitin and a mutant ALS-linked SOD1 protein correlate with disease progression and fragmentation of the Golgi apparatus. Journal of the neurological sciences. vol 173. issue 1. 2000-04-13. PMID:10675580. transgenic mice that express the g93a mutation of human cu,zn superoxide dismutase (sod1(g93a)), found in familial amyotrophic lateral sclerosis (fals), showed clinical symptoms and histopathological changes of sporadic als, including fragmentation of the neuronal golgi apparatus (ga). 2000-04-13 2023-08-12 mouse
A Stieber, J O Gonatas, J Collard, J Meier, J Julien, P Schweitzer, N K Gonata. The neuronal Golgi apparatus is fragmented in transgenic mice expressing a mutant human SOD1, but not in mice expressing the human NF-H gene. Journal of the neurological sciences. vol 173. issue 1. 2000-04-13. PMID:10675581. fragmentation of the golgi apparatus (ga) of motor neurons was first described in sporadic amyotrophic lateral sclerosis (als) and later confirmed in transgenic mice expressing the g93a mutation of the gene encoding the enzyme cu,zn superoxide dismutase (sod1(g93a)) found in some cases of familial als. 2000-04-13 2023-08-12 mouse
K Kikugawa, R Nakano, T Inuzuka, Y Kokubo, Y Narita, S Kuzuhara, S Yoshida, S Tsuj. A missense mutation in the SOD1 gene in patients with amyotrophic lateral sclerosis from the Kii Peninsula and its vicinity, Japan. Neurogenetics. vol 1. issue 2. 2000-04-12. PMID:10732812. a missense mutation in the sod1 gene in patients with amyotrophic lateral sclerosis from the kii peninsula and its vicinity, japan. 2000-04-12 2023-08-12 Not clear
J Kong, Z X. Overexpression of neurofilament subunit NF-L and NF-H extends survival of a mouse model for amyotrophic lateral sclerosis. Neuroscience letters. vol 281. issue 1. 2000-04-11. PMID:10686419. mutations in superoxide dismutase 1 (sod1) cause amyotrophic lateral sclerosis (als) in a subset of patients. 2000-04-11 2023-08-12 mouse
J S Zu, H X Deng, T P Lo, H Mitsumoto, M S Ahmed, W Y Hung, Z J Cai, J A Tainer, T Siddiqu. Exon 5 encoded domain is not required for the toxic function of mutant SOD1 but essential for the dismutase activity: identification and characterization of two new SOD1 mutations associated with familial amyotrophic lateral sclerosis. Neurogenetics. vol 1. issue 1. 2000-04-11. PMID:10735277. exon 5 encoded domain is not required for the toxic function of mutant sod1 but essential for the dismutase activity: identification and characterization of two new sod1 mutations associated with familial amyotrophic lateral sclerosis. 2000-04-11 2023-08-12 Not clear
J S Zu, H X Deng, T P Lo, H Mitsumoto, M S Ahmed, W Y Hung, Z J Cai, J A Tainer, T Siddiqu. Exon 5 encoded domain is not required for the toxic function of mutant SOD1 but essential for the dismutase activity: identification and characterization of two new SOD1 mutations associated with familial amyotrophic lateral sclerosis. Neurogenetics. vol 1. issue 1. 2000-04-11. PMID:10735277. two new mutations in the gene encoding cytoplasmic cu,zn superoxide dismutase (sod1) have been discovered in patients with familial amyotrophic lateral sclerosis (fals). 2000-04-11 2023-08-12 Not clear
G M Alexander, J S Deitch, J L Seeburger, L Del Valle, T D Heiman-Patterso. Elevated cortical extracellular fluid glutamate in transgenic mice expressing human mutant (G93A) Cu/Zn superoxide dismutase. Journal of neurochemistry. vol 74. issue 4. 2000-04-11. PMID:10737625. transgenic mice expressing a mutated (g93a) human cu/zn superoxide dismutase (sod1) develop motor neuron pathology and clinical symptoms similar to those seen in patients with amyotrophic lateral sclerosis. 2000-04-11 2023-08-12 mouse