PubMed:17114818 JSON TXT

Annnotations TAB JSON ListView MergeView

sonoma2

sonoma

{"project":"sonoma","denotations":[{"id":"T-0","span":{"begin":16,"end":33},"obj":"GENE"},{"id":"T-1","span":{"begin":120,"end":122},"obj":"GENE"},{"id":"T-2","span":{"begin":176,"end":180},"obj":"VAR"},{"id":"T-3","span":{"begin":181,"end":185},"obj":"GENE"},{"id":"T-4","span":{"begin":270,"end":273},"obj":"DISEASE"},{"id":"T-5","span":{"begin":310,"end":317},"obj":"REG"},{"id":"T-6","span":{"begin":335,"end":339},"obj":"GENE"},{"id":"T-7","span":{"begin":427,"end":438},"obj":"REG"},{"id":"T-8","span":{"begin":495,"end":501},"obj":"GENE"},{"id":"T-9","span":{"begin":511,"end":518},"obj":"REG"},{"id":"T-10","span":{"begin":552,"end":563},"obj":"REG"},{"id":"T-11","span":{"begin":587,"end":590},"obj":"DISEASE"},{"id":"T-12","span":{"begin":627,"end":631},"obj":"GENE"},{"id":"T-13","span":{"begin":636,"end":642},"obj":"GENE"},{"id":"T-14","span":{"begin":648,"end":655},"obj":"REG"},{"id":"T-15","span":{"begin":675,"end":685},"obj":"REG"},{"id":"T-16","span":{"begin":721,"end":725},"obj":"GENE"},{"id":"T-17","span":{"begin":760,"end":766},"obj":"GENE"},{"id":"T-18","span":{"begin":820,"end":831},"obj":"REG"},{"id":"T-19","span":{"begin":919,"end":923},"obj":"GENE"},{"id":"T-20","span":{"begin":1052,"end":1056},"obj":"GENE"},{"id":"T-21","span":{"begin":1078,"end":1084},"obj":"GENE"},{"id":"T-22","span":{"begin":1097,"end":1107},"obj":"REG"},{"id":"T-23","span":{"begin":1135,"end":1138},"obj":"DISEASE"},{"id":"T-24","span":{"begin":1240,"end":1251},"obj":"REG"}],"relations":[{"id":"R-0","pred":"ThemeOf","subj":"T-1","obj":"T-4"},{"id":"R-1","pred":"ThemeOf","subj":"T-2","obj":"T-3"},{"id":"R-2","pred":"ThemeOf","subj":"T-3","obj":"T-4"},{"id":"R-3","pred":"ThemeOf","subj":"T-6","obj":"T-7"},{"id":"R-4","pred":"ThemeOf","subj":"T-10","obj":"T-11"},{"id":"R-5","pred":"ThemeOf","subj":"T-13","obj":"T-14"},{"id":"R-6","pred":"ThemeOf","subj":"T-20","obj":"T-23"},{"id":"R-7","pred":"ThemeOf","subj":"T-21","obj":"T-22"},{"id":"R-8","pred":"ThemeOf","subj":"T-21","obj":"T-23"},{"id":"R-9","pred":"ThemeOf","subj":"T-22","obj":"T-23"}],"text":"Upregulation of metallothionein-I mRNA expression in a rodent model for amyotrophic lateral sclerosis.\nMetallothionein (MT) mRNA expression was investigated in a rodent model (G93A SOD1 transgenic mouse) for a lethal motor neuron disease, amyotrophic lateral sclerosis (ALS). In 8-wk-old mice that did not yet exhibit motor paralysis, MT-I mRNA expression was already significantly upregulated in the region of the spinal cord responsible for motor paralysis. The expression of another isoform, MT-III, was not changed. In the cerebellum, which is not responsible for motor paralysis in ALS, neither the expression profiles of MT-I nor MT-III were altered. In 16-wk-old mice exhibiting motor paralysis, the expression of MT-I mRNA remained upregulated and the MT-III level tended to be elevated. Although no significant differences were found in the levels of both isoforms in the liver or kidney of 8-wk-old mice, the MT-I mRNA expression level was significantly upregulated in the kidney and liver of 16-wk-old mice. These results indicated that the MT-I isoform, but not the MT-III isoform, is associated with motor neuron death in ALS and suggested that the disease might be a systemic disorder to which the spinal cord is particularly susceptible."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":239,"end":268},"obj":"HP_0007354"},{"id":"T2","span":{"begin":239,"end":250},"obj":"HP_0003202"},{"id":"T3","span":{"begin":324,"end":333},"obj":"HP_0003470"},{"id":"T4","span":{"begin":449,"end":458},"obj":"HP_0003470"},{"id":"T5","span":{"begin":574,"end":583},"obj":"HP_0003470"},{"id":"T6","span":{"begin":692,"end":701},"obj":"HP_0003470"},{"id":"T7","span":{"begin":1190,"end":1223},"obj":"HP_0002143"},{"id":"T8","span":{"begin":1190,"end":1218},"obj":"HP_0008443"}],"text":"Upregulation of metallothionein-I mRNA expression in a rodent model for amyotrophic lateral sclerosis.\nMetallothionein (MT) mRNA expression was investigated in a rodent model (G93A SOD1 transgenic mouse) for a lethal motor neuron disease, amyotrophic lateral sclerosis (ALS). In 8-wk-old mice that did not yet exhibit motor paralysis, MT-I mRNA expression was already significantly upregulated in the region of the spinal cord responsible for motor paralysis. The expression of another isoform, MT-III, was not changed. In the cerebellum, which is not responsible for motor paralysis in ALS, neither the expression profiles of MT-I nor MT-III were altered. In 16-wk-old mice exhibiting motor paralysis, the expression of MT-I mRNA remained upregulated and the MT-III level tended to be elevated. Although no significant differences were found in the levels of both isoforms in the liver or kidney of 8-wk-old mice, the MT-I mRNA expression level was significantly upregulated in the kidney and liver of 16-wk-old mice. These results indicated that the MT-I isoform, but not the MT-III isoform, is associated with motor neuron death in ALS and suggested that the disease might be a systemic disorder to which the spinal cord is particularly susceptible."}

PubMed:17114818 JSONTXT

Annnotations TAB JSON ListView MergeView

sonoma2

sonoma

PubmedHPO

PubMed:17114818 JSON TXT