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model of classic MSUD was created by gene knockout of the E2 subunit of BCKDH. The phenotype of these knockout animals is strikingly similar to humans with classic MSUD. Knockout mice were born at the expected frequency and appeared normal at birth. Within a day of birth and following suckling, blood levels of BCAA were markedly elevated. Concomitantly, levels of the amino acids alanine, glutamate, and glutamine, whose synthesis is linked with normal metabolism of BCAA, were decreased (Table 1). The activity of BCKDH in livers of homozygous knockout mouse pups was undetectable, accounting for the accumulation of unmetabolized BCAA. Immunoreactive E2 protein was absent in liver and fibroblasts of homozygous pups. The phenotypic behavior of homozygous mouse pups resembles symptoms seen in newborn classic MSUD patients. These include signs of neurologic dysfunction such as seizures, stupor, lethargy, loss of motor activity, and respiratory difficulties [1]. These neurologic symptoms may result from reduced levels of glutamate, glutamine, alanine, and other similar neuroactive amino acids, which are considered the culprit for MSUD encephalopathies in patients [1,37]. Finally, nearly all of the homozygous pups died within 72 hours of birth. This neonatal lethality is likely due to the accumulation of BCAA to neurotoxic levels, ketoacidosis, brain edema, dehydration, and malnutrition as observed in the MSUD calf [17] and in classic MSUD patients [1]. Heterozygous knockouts were normal and had normal levels of BCAA despite having approximately half of BCKDH enzymatic activity. From the characterization studies completed thus far, the null mutation mouse accurately represents a model of classic MSUD and appears to be a faithful model of the human disease with respect to several biochemical phenotypes [1]."}

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The phenotype of these knockout animals is strikingly similar to humans with classic MSUD. Knockout mice were born at the expected frequency and appeared normal at birth. Within a day of birth and following suckling, blood levels of BCAA were markedly elevated. Concomitantly, levels of the amino acids alanine, glutamate, and glutamine, whose synthesis is linked with normal metabolism of BCAA, were decreased (Table 1). The activity of BCKDH in livers of homozygous knockout mouse pups was undetectable, accounting for the accumulation of unmetabolized BCAA. Immunoreactive E2 protein was absent in liver and fibroblasts of homozygous pups. The phenotypic behavior of homozygous mouse pups resembles symptoms seen in newborn classic MSUD patients. These include signs of neurologic dysfunction such as seizures, stupor, lethargy, loss of motor activity, and respiratory difficulties [1]. These neurologic symptoms may result from reduced levels of glutamate, glutamine, alanine, and other similar neuroactive amino acids, which are considered the culprit for MSUD encephalopathies in patients [1,37]. Finally, nearly all of the homozygous pups died within 72 hours of birth. This neonatal lethality is likely due to the accumulation of BCAA to neurotoxic levels, ketoacidosis, brain edema, dehydration, and malnutrition as observed in the MSUD calf [17] and in classic MSUD patients [1]. Heterozygous knockouts were normal and had normal levels of BCAA despite having approximately half of BCKDH enzymatic activity. From the characterization studies completed thus far, the null mutation mouse accurately represents a model of classic MSUD and appears to be a faithful model of the human disease with respect to several biochemical phenotypes [1]."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T19543","span":{"begin":659,"end":661},"obj":"PR:000006300"},{"id":"T19542","span":{"begin":638,"end":642},"obj":"CHEBI:22918"},{"id":"T19541","span":{"begin":626,"end":637},"obj":"GO:0008152"},{"id":"T19540","span":{"begin":560,"end":565},"obj":"NCBITaxon:10088"},{"id":"T19539","span":{"begin":530,"end":536},"obj":"UBERON:0002107"},{"id":"T19538","span":{"begin":473,"end":477},"obj":"CHEBI:22918"},{"id":"T19537","span":{"begin":459,"end":477},"obj":"GO:0009081"},{"id":"T19536","span":{"begin":316,"end":320},"obj":"CHEBI:22918"},{"id":"T19535","span":{"begin":300,"end":305},"obj":"UBERON:0000178"},{"id":"T19534","span":{"begin":290,"end":298},"obj":"GO:0001967"},{"id":"T19533","span":{"begin":270,"end":275},"obj":"GO:0007567"},{"id":"T19532","span":{"begin":247,"end":252},"obj":"GO:0007567"},{"id":"T19531","span":{"begin":193,"end":197},"obj":"GO:0007567"},{"id":"T19530","span":{"begin":183,"end":187},"obj":"NCBITaxon:10088"},{"id":"T19529","span":{"begin":148,"end":154},"obj":"NCBITaxon:9606"},{"id":"T19528","span":{"begin":115,"end":122},"obj":"NCBITaxon:33208"},{"id":"T19527","span":{"begin":62,"end":81},"obj":"PR:000006300"},{"id":"T19526","span":{"begin":41,"end":45},"obj":"SO:0000704"},{"id":"T19556","span":{"begin":1767,"end":1772},"obj":"NCBITaxon:9606"},{"id":"T19555","span":{"begin":1673,"end":1678},"obj":"NCBITaxon:10088"},{"id":"T19554","span":{"begin":1533,"end":1537},"obj":"CHEBI:22918"},{"id":"T19553","span":{"begin":1362,"end":1367},"obj":"UBERON:0000955"},{"id":"T19552","span":{"begin":1321,"end":1325},"obj":"CHEBI:22918"},{"id":"T19551","span":{"begin":1253,"end":1258},"obj":"GO:0007567"},{"id":"T19550","span":{"begin":1229,"end":1233},"obj":"GO:0016265"},{"id":"T19549","span":{"begin":979,"end":989},"obj":"UBERON:0001016"},{"id":"T19548","span":{"begin":943,"end":954},"obj":"UBERON:0001004"},{"id":"T19547","span":{"begin":856,"end":866},"obj":"UBERON:0001016"},{"id":"T19546","span":{"begin":764,"end":769},"obj":"NCBITaxon:10088"},{"id":"T19545","span":{"begin":694,"end":705},"obj":"CL:0000057"},{"id":"T19544","span":{"begin":684,"end":689},"obj":"UBERON:0002107"}],"text":"Our model of classic MSUD was created by gene knockout of the E2 subunit of BCKDH. The phenotype of these knockout animals is strikingly similar to humans with classic MSUD. Knockout mice were born at the expected frequency and appeared normal at birth. Within a day of birth and following suckling, blood levels of BCAA were markedly elevated. Concomitantly, levels of the amino acids alanine, glutamate, and glutamine, whose synthesis is linked with normal metabolism of BCAA, were decreased (Table 1). The activity of BCKDH in livers of homozygous knockout mouse pups was undetectable, accounting for the accumulation of unmetabolized BCAA. Immunoreactive E2 protein was absent in liver and fibroblasts of homozygous pups. The phenotypic behavior of homozygous mouse pups resembles symptoms seen in newborn classic MSUD patients. These include signs of neurologic dysfunction such as seizures, stupor, lethargy, loss of motor activity, and respiratory difficulties [1]. These neurologic symptoms may result from reduced levels of glutamate, glutamine, alanine, and other similar neuroactive amino acids, which are considered the culprit for MSUD encephalopathies in patients [1,37]. Finally, nearly all of the homozygous pups died within 72 hours of birth. This neonatal lethality is likely due to the accumulation of BCAA to neurotoxic levels, ketoacidosis, brain edema, dehydration, and malnutrition as observed in the MSUD calf [17] and in classic MSUD patients [1]. Heterozygous knockouts were normal and had normal levels of BCAA despite having approximately half of BCKDH enzymatic activity. From the characterization studies completed thus far, the null mutation mouse accurately represents a model of classic MSUD and appears to be a faithful model of the human disease with respect to several biochemical phenotypes [1]."}