| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| C K Hand, V Mayeux-Portas, J Khoris, V Briolotti, P Clavelou, W Camu, G A Roulea. Compound heterozygous D90A and D96N SOD1 mutations in a recessive amyotrophic lateral sclerosis family. Annals of neurology. vol 49. issue 2. 2001-03-29. PMID:11220750. |
compound heterozygous d90a and d96n sod1 mutations in a recessive amyotrophic lateral sclerosis family. |
2001-03-29 |
2023-08-12 |
Not clear |
| C K Hand, V Mayeux-Portas, J Khoris, V Briolotti, P Clavelou, W Camu, G A Roulea. Compound heterozygous D90A and D96N SOD1 mutations in a recessive amyotrophic lateral sclerosis family. Annals of neurology. vol 49. issue 2. 2001-03-29. PMID:11220750. |
we describe a french amyotrophic lateral sclerosis (als) family with two distinct mutations in the cu/zn superoxide dismutase (sod1) gene. |
2001-03-29 |
2023-08-12 |
Not clear |
| M Lee, D Hyun, P Jenner, B Halliwel. Effect of overexpression of wild-type and mutant Cu/Zn-superoxide dismutases on oxidative damage and antioxidant defences: relevance to Down's syndrome and familial amyotrophic lateral sclerosis. Journal of neurochemistry. vol 76. issue 4. 2001-03-22. PMID:11181815. |
transfection of these cell lines with dna encoding two mutant sod1 enzymes (g37r and g85r) associated with familial amyotrophic lateral sclerosis (fals), produced similar, but more severe changes, i.e. |
2001-03-22 |
2023-08-12 |
mouse |
| D Hoyaux, J Alao, J Fuchs, R Kiss, B Keller, C W Heizmann, R Pochet, D Frerman. S100A6, a calcium- and zinc-binding protein, is overexpressed in SOD1 mutant mice, a model for amyotrophic lateral sclerosis. Biochimica et biophysica acta. vol 1498. issue 2-3. 2001-02-15. PMID:11108968. |
s100a6, a calcium- and zinc-binding protein, is overexpressed in sod1 mutant mice, a model for amyotrophic lateral sclerosis. |
2001-02-15 |
2023-08-12 |
mouse |
| D Jaarsma, E D Haasdijk, J A Grashorn, R Hawkins, W van Duijn, H W Verspaget, J London, J C Holsteg. Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1. Neurobiology of disease. vol 7. issue 6 Pt B. 2001-02-15. PMID:11114261. |
human cu/zn superoxide dismutase (sod1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant sod1. |
2001-02-15 |
2023-08-12 |
mouse |
| D Jaarsma, E D Haasdijk, J A Grashorn, R Hawkins, W van Duijn, H W Verspaget, J London, J C Holsteg. Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1. Neurobiology of disease. vol 7. issue 6 Pt B. 2001-02-15. PMID:11114261. |
mutations in the sod1 gene cause a familial form of amyotrophic lateral sclerosis (fals). |
2001-02-15 |
2023-08-12 |
mouse |
| S M Winter, A Claus, C Oberwittler, H Völkel, S Wenzler, A C Ludolp. Recessively inherited amyotrophic lateral sclerosis: a Germany family with the D90A CuZn-SOD mutation. Journal of neurology. vol 247. issue 10. 2001-02-15. PMID:11127534. |
mutations of the sod1 gene encoding the free radical scavenging enzyme copper-zinc superoxide dismutase (cuzn-sod) occur in patients with familial amyotrophic lateral sclerosis (als). |
2001-02-15 |
2023-08-12 |
Not clear |
| C B Kunst, L Messer, J Gordon, J Haines, D Patterso. Genetic mapping of a mouse modifier gene that can prevent ALS onset. Genomics. vol 70. issue 2. 2001-02-08. PMID:11112346. |
mutations in the cytoplasmic cu/zn superoxide dismutase (sod1) gene on human chromosome 21q22.1 cause 10-20% of familial amyotrophic lateral sclerosis (als) cases. |
2001-02-08 |
2023-08-12 |
mouse |
| S Kato, S Horiuchi, J Liu, D W Cleveland, N Shibata, K Nakashima, R Nagai, A Hirano, M Takikawa, M Kato, I Nakano, E Oham. Advanced glycation endproduct-modified superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice expressing human SOD1 with a G85R mutation. Acta neuropathologica. vol 100. issue 5. 2001-02-01. PMID:11045671. |
advanced glycation endproduct-modified superoxide dismutase-1 (sod1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with sod1 gene mutations and transgenic mice expressing human sod1 with a g85r mutation. |
2001-02-01 |
2023-08-12 |
mouse |
| S Kato, S Horiuchi, J Liu, D W Cleveland, N Shibata, K Nakashima, R Nagai, A Hirano, M Takikawa, M Kato, I Nakano, E Oham. Advanced glycation endproduct-modified superoxide dismutase-1 (SOD1)-positive inclusions are common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutations and transgenic mice expressing human SOD1 with a G85R mutation. Acta neuropathologica. vol 100. issue 5. 2001-02-01. PMID:11045671. |
to clarify the biological significance of the neuronal lewy body-like hyaline inclusions and astrocytic hyaline inclusions characteristically found in patients with familial amyotrophic lateral sclerosis with superoxide dismutase-1 (sod1) gene mutations and in transgenic mice expressing human sod1 with g85r mutation, the detailed protein composition in both types of inclusions was immunohistochemically analyzed using 45 different antibodies. |
2001-02-01 |
2023-08-12 |
mouse |
| J H Kang, W S Eu. Enhanced oxidative damage by the familial amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutants. Biochimica et biophysica acta. vol 1524. issue 2-3. 2001-01-25. PMID:11113563. |
some cases of familial amyotrophic lateral sclerosis (fals), a degenerative disorder of motor neurons, is associated with mutation in the cu,zn-superoxide dismutase (sod) gene sod1. |
2001-01-25 |
2023-08-12 |
Not clear |
| A Kawata, S Kato, T Shimizu, H Hayashi, S Hirai, H Misawa, R Takahash. Aberrant splicing of human Cu/Zn superoxide dismutase (SOD1) RNA transcripts. Neuroreport. vol 11. issue 12. 2001-01-18. PMID:10976937. |
two abnormal sod1 mrnas, exon 2-skipping and exon 2 and 3-skipping species, were identified from occipital brain tissue of sporadic amyotrophic lateral sclerosis (als) patients carrying no mutations in the sod1 gene. |
2001-01-18 |
2023-08-12 |
human |
| R Chen, N End. The potential for the use of mononuclear cells from human umbilical cord blood in the treatment of amyotrophic lateral sclerosis in SOD1 mice. Journal of medicine. vol 31. issue 1-2. 2001-01-11. PMID:10998753. |
the potential for the use of mononuclear cells from human umbilical cord blood in the treatment of amyotrophic lateral sclerosis in sod1 mice. |
2001-01-11 |
2023-08-12 |
mouse |
| R Chen, N End. The potential for the use of mononuclear cells from human umbilical cord blood in the treatment of amyotrophic lateral sclerosis in SOD1 mice. Journal of medicine. vol 31. issue 1-2. 2001-01-11. PMID:10998753. |
the sod1 mice (transgenic b6sjl-tgn(sod1-g93a)1gur) have a mutation of the human transgene (cuzn superoxide dismutase gene sod1) that has been associated with amyotrophic lateral sclerosis (als). |
2001-01-11 |
2023-08-12 |
mouse |
| J Prudlo, J Koenig, J Gräser, E Burckhardt, P Mestres, M Menger, K Roeme. Motor neuron cell death in a mouse model of FALS is not mediated by the p53 cell survival regulator. Brain research. vol 879. issue 1-2. 2000-12-14. PMID:11011020. |
mutant cu/zn superoxide dismutase (sod1) associated with familial amyotrophic lateral sclerosis (fals) causes selective motor neuron loss through unknown mechanisms of cell damage. |
2000-12-14 |
2023-08-12 |
mouse |
| J R Hall, C A Strathde. Disease-associated mutations in SOD1 are impervious to dominant positive or negative effects. Biochemical and biophysical research communications. vol 276. issue 3. 2000-11-21. PMID:11027589. |
the familial form of amyotrophic lateral sclerosis is caused by mutations in the sod1 gene encoding the cytosolic antioxidant enzyme cu,zn superoxide dismutase. |
2000-11-21 |
2023-08-12 |
Not clear |
| M Hirano, W Y Hung, N Cole, A C Azim, H X Deng, T Siddiqu. Multiple transcripts of the human Cu,Zn superoxide dismutase gene. Biochemical and biophysical research communications. vol 276. issue 1. 2000-10-26. PMID:11006081. |
we have identified five alternatively spliced transcripts of the gene for human cu,zn superoxide dismutase (sod1), a causative gene for autosomal dominant amyotrophic lateral sclerosis (als). |
2000-10-26 |
2023-08-12 |
human |
| A Stieber, J O Gonatas, N K Gonata. Aggregates of mutant protein appear progressively in dendrites, in periaxonal processes of oligodendrocytes, and in neuronal and astrocytic perikarya of mice expressing the SOD1(G93A) mutation of familial amyotrophic lateral sclerosis. Journal of the neurological sciences. vol 177. issue 2. 2000-10-23. PMID:10980307. |
aggregates of mutant protein appear progressively in dendrites, in periaxonal processes of oligodendrocytes, and in neuronal and astrocytic perikarya of mice expressing the sod1(g93a) mutation of familial amyotrophic lateral sclerosis. |
2000-10-23 |
2023-08-12 |
mouse |
| A Stieber, J O Gonatas, N K Gonata. Aggregates of mutant protein appear progressively in dendrites, in periaxonal processes of oligodendrocytes, and in neuronal and astrocytic perikarya of mice expressing the SOD1(G93A) mutation of familial amyotrophic lateral sclerosis. Journal of the neurological sciences. vol 177. issue 2. 2000-10-23. PMID:10980307. |
mice expressing the g93a and other mutations of cu,zn superoxide dismutase (sod1(g93a)) are valid models for the familial form of amyotrophic lateral sclerosis (fals) with sod1 mutations and, probably, for sporadic als. |
2000-10-23 |
2023-08-12 |
mouse |
| J L González de Aguilar, J W Gordon, F René, M de Tapia, B Lutz-Bucher, C Gaiddon, J P Loeffle. Alteration of the Bcl-x/Bax ratio in a transgenic mouse model of amyotrophic lateral sclerosis: evidence for the implication of the p53 signaling pathway. Neurobiology of disease. vol 7. issue 4. 2000-10-11. PMID:10964611. |
molecular mechanisms promoting neuronal death in amyotrophic lateral sclerosis (als) were investigated using transgenic mice that overexpressed the g86r mutated form of the cu/zn superoxide dismutase (sod1) gene. |
2000-10-11 |
2023-08-12 |
mouse |