Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the mRNA levels during mammalian myogenesis were compared for seven polypeptides of mitochondrial respiration (the mitochondrial DNA-encoded cytochrome oxidase subunit III, ATP synthase subunit 6, NADH dehydrogenase subunits 1 and 2, and 16S ribosomal RNA; the nuclear encoded ATP synthase beta subunit and the adenine nucleotide translocase) and three polypeptides of glycolysis (glyceraldehyde-3-phosphate dehydrogenase, pyruvate kinase, and triose-phosphate isomerase). Progressive changes during the conversion from myoblasts to myotubes were monitored under both atmospheric oxygen (normoxic) and hypoxic environments. Northern analyses revealed coordinate, biphasic, and reciprocal expression of the respiratory and glycolytic mRNAs during myogenesis. In normoxic cells the mitochondrial respiratory enzymes were highest in myoblasts, declined 3- to 5-fold during commitment and exist from the cell cycle, and increased progressively as the myotubes matured. By contrast, the glycolytic enzyme mRNAs rose 3- to 6-fold on commitment and then progressively declined. When partially differentiated myotubes were switched to hypoxic conditions, the glycolytic enzyme mRNAs increased and the respiratory mRNAs declined. Hence, the developmental regulation of muscle bioenergetic metabolism appears to be regulated at the pretranslational level and is modulated by oxygen tension.
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PMID:Coordinate reciprocal trends in glycolytic and mitochondrial transcript accumulations during the in vitro differentiation of human myoblasts. 213 61

Treatment of rats with hydroxycobalamin[c-lactam] (HCCL), a cobalamin antagonist, results in both increased hepatic mitochondrial content and the development of defects in mitochondrial ubiquinol:cytochrome c oxidoreductase and cytochrome c oxidase. The present study was designed to evaluate changes in hepatic mitochondrial RNA contents in response to HCCL treatment in rats. After 2 weeks of HCCL treatment, hepatic contents of the mature mitochondrial mRNAs (expressed normalized to 28 S rRNA) encoding subunit II of cytochrome c oxidase (CO II), subunit 1 of NADH dehydrogenase (ND1), and cytochrome b were reduced to values 40-60% of those observed in RNA from control liver tissue. In addition, HCCL induced a pronounced accumulation of high molecular weight RNA species which hybridized to mitochondrial probes and represented polycistronic RNA sequences. The polycistronic RNAs were products of the heavy strand of the mitochondrial genome, and major species demonstrated hybridization patterns consistent with identifications corresponding to the 12-16 S rRNA, 12-16 S-ND1, 16 S-ND1, and CO II-ATP synthase subunit 6 regions of the mitochondrial genome. Maximal expression of the polycistronic mitochondrial RNA was observed after 2 weeks of HCCL treatment. Thus, HCCL treatment interferes with mitochondrial RNA processing and decreases the content of mature mitochondrial mRNAs. Altered expression of the mitochondrial genome may be responsible for the decreased electron transport chain activity known to result from HCCL administration.
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PMID:Hepatic cobalamin deficiency induced by hydroxycobalamin[c-lactam] treatment in rats is associated with decreased mitochondrial mRNA contents and accumulation of polycistronic mitochondrial RNAs. 750 36