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PubMed:12215229 JSONTXT

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DisGeNET

Id Subject Object Predicate Lexical cue
T0 28-32 gene:6647 denotes SOD1
T1 171-177 disease:C3825627 denotes stress
T2 28-32 gene:6647 denotes SOD1
T3 100-103 disease:C0002736 denotes ALS
T4 0-26 gene:6647 denotes Cu/Zn superoxide dismutase
T5 60-98 disease:C1862939 denotes familial amyotrophic lateral sclerosis
T6 0-26 gene:6647 denotes Cu/Zn superoxide dismutase
T7 100-103 disease:C0002736 denotes ALS
T8 28-32 gene:6647 denotes SOD1
T9 60-98 disease:C1862939 denotes familial amyotrophic lateral sclerosis
T10 0-26 gene:6647 denotes Cu/Zn superoxide dismutase
T11 171-177 disease:C3825627 denotes stress
T12 1020-1024 gene:6647 denotes SOD1
T13 946-949 disease:C0002736 denotes ALS
T14 1020-1024 gene:6647 denotes SOD1
T15 906-944 disease:C1862939 denotes familial amyotrophic lateral sclerosis
R1 T0 T1 associated_with SOD1,stress
R2 T2 T3 associated_with SOD1,ALS
R3 T4 T5 associated_with Cu/Zn superoxide dismutase,familial amyotrophic lateral sclerosis
R4 T6 T7 associated_with Cu/Zn superoxide dismutase,ALS
R5 T8 T9 associated_with SOD1,familial amyotrophic lateral sclerosis
R6 T10 T11 associated_with Cu/Zn superoxide dismutase,stress
R7 T12 T13 associated_with SOD1,ALS
R8 T14 T15 associated_with SOD1,familial amyotrophic lateral sclerosis

DisGeNET5_gene_disease

Id Subject Object Predicate Lexical cue
12215229-0#0#26#gene6647 0-26 gene6647 denotes Cu/Zn superoxide dismutase
12215229-0#28#32#gene6647 28-32 gene6647 denotes SOD1
12215229-0#69#98#diseaseC0002736 69-98 diseaseC0002736 denotes amyotrophic lateral sclerosis
12215229-0#100#103#diseaseC0002736 100-103 diseaseC0002736 denotes ALS
12215229-0#69#98#diseaseC0002736 69-98 diseaseC0002736 denotes amyotrophic lateral sclerosis
12215229-0#100#103#diseaseC0002736 100-103 diseaseC0002736 denotes ALS
0#26#gene664769#98#diseaseC0002736 12215229-0#0#26#gene6647 12215229-0#69#98#diseaseC0002736 associated_with Cu/Zn superoxide dismutase,amyotrophic lateral sclerosis
0#26#gene6647100#103#diseaseC0002736 12215229-0#0#26#gene6647 12215229-0#100#103#diseaseC0002736 associated_with Cu/Zn superoxide dismutase,ALS
0#26#gene664769#98#diseaseC0002736 12215229-0#0#26#gene6647 12215229-0#69#98#diseaseC0002736 associated_with Cu/Zn superoxide dismutase,amyotrophic lateral sclerosis
0#26#gene6647100#103#diseaseC0002736 12215229-0#0#26#gene6647 12215229-0#100#103#diseaseC0002736 associated_with Cu/Zn superoxide dismutase,ALS
28#32#gene664769#98#diseaseC0002736 12215229-0#28#32#gene6647 12215229-0#69#98#diseaseC0002736 associated_with SOD1,amyotrophic lateral sclerosis
28#32#gene6647100#103#diseaseC0002736 12215229-0#28#32#gene6647 12215229-0#100#103#diseaseC0002736 associated_with SOD1,ALS
28#32#gene664769#98#diseaseC0002736 12215229-0#28#32#gene6647 12215229-0#69#98#diseaseC0002736 associated_with SOD1,amyotrophic lateral sclerosis
28#32#gene6647100#103#diseaseC0002736 12215229-0#28#32#gene6647 12215229-0#100#103#diseaseC0002736 associated_with SOD1,ALS

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 193-732 BACKGROUND denotes The exact molecular mechanisms by which mutations in Cu/Zn superoxide dismutase (SOD1) cause motor neuron injury remain incompletely understood, though a body of evidence suggests that the mutant protein exerts a cell-specific toxic gain of function. The role of nitric oxide (NO) in SOD1-related motor neuron injury has been particularly controversial. Theoretically, there are arguments to suggest that NO may exert an important role in motor neuron injury, but there is relatively little direct experimental support for this hypothesis.
T2 745-859 OBJECTIVE denotes The present study aimed to examine further the potential role for NO in motor neuron injury caused by mutant SOD1.
T3 868-1336 METHODS denotes We have generated a cellular model of familial amyotrophic lateral sclerosis (ALS) by stably transfecting NSC34 cells with one of three mutant forms of SOD1 (G93A, G37R, I113T). In the presence of mutant SOD1, NSC34 cells show increased cell death following oxidative stress induced by serum withdrawal. This model of motor neuron death involves cellular release of superoxide and NO radicals, which were directly measured in real time using microelectrode biosensors.
T4 1346-2027 RESULTS denotes The expression of both normal and mutant SOD1 decreased the measured extracellular superoxide release, but had divergent effects on the measured release of NO. Normal SOD1 increased the measured NO release, whereas cells expressing mutant SOD1 released less NO. Co-administration of two different nitric oxide synthase inhibitors (L-NAME and L-N-methyl arginine) did show some neuroprotective effect, but this was only partial, and the effect was more marked using nuclear integrity as a measure of cell viability, rather than MTT conversion. Cells expressing mutant SOD1 were, however, more sensitive to toxicity induced by extrinsic exposure to NO, using a slow-release NO donor.
T5 2040-2173 CONCLUSIONS denotes NO is likely to contribute to motor neuron injury, but this does not fully account for all the cellular toxic effects of mutant SOD1.