Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fish electric organ is a skeletal muscle homolog in which many muscle-specific genes are inhibited while acetylcholine receptor is expressed at high levels. The molecular mechanisms underlying this discoordinate regulation have not yet been explored. We have obtained partial sequences for MyoD, myogenin, and myf5 from Torpedo californica and have measured their mRNAs in several organs, using ribonuclease protection. We have found that MyoD and myf5 are expressed at comparable levels in muscle and electric organ, whereas myogenin transcripts could not be detected in either tissue. Acetylcholine receptor alpha subunit mRNA, on the other hand, is two orders of magnitude more abundant in electric tissue. We conclude that neither the loss of contractile proteins from, nor the enhanced expression of acetylcholine receptor genes in, the differentiating electrocyte is a simple consequence of the abundance of myogenic factor messages.
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PMID:Expression of myogenic factors in skeletal muscle and electric organ of Torpedo californica. 132 28

1. We have prepared probes specific for the chicken myogenic determination genes MyoD, myogenin, myf5, and herculin and have investigated the expression of these genes in response to denervation and acute electrical stimulation in neonate chick muscle, using ribonuclease protection. 2. Upon denervation, herculin mRNA remains essentially unchanged, myf5 transcript levels approximately double, and MyoD message is up-regulated by two- to fivefold. In contrast, the message coding for myogenin, barely detectable in innervated muscle, rises dramatically (approximately 200-fold) on the second day after nerve section; in this respect it resembles acetylcholine receptor (AChR) alpha-, gamma- and delta-subunit mRNAs. Cohybridization experiments reveal that the increase in myogenin mRNA slightly precedes the rise in AChR alpha-subunit message. 3. Electrical stimulation of denervated muscle leads to an immediate decline in myogenin and AChR alpha-subunit mRNAs, with half-lives of less than an hour and approximately 4 hr, respectively; message stability measurements suggest that this is effected through a rapid shutdown of transcription. Messages coding for MyoD, myf5, and herculin decay much more slowly, as a result of slower turnover. 4. Previous experiments have indicated the involvement of a de novo induced (Tsay, H.-J., Neville, C. M., and Schmidt, J., FEBS Lett. 274:69-72, 1990) autocatalytic (Neville, C. M., Schmidt, M., and Schmidt, J., NeuroReport 2:655-657, 1991) transcription factor in the denervation-triggered up-regulation of AChR alpha-subunit expression; the denervation and electrical stimulation experiments reported here are compatible with the notion that myogenin is that factor.
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PMID:Response of myogenic determination factors to cessation and resumption of electrical activity in skeletal muscle: a possible role for myogenin in denervation supersensitivity. 133 17

The transcriptional activity of the acetylcholine receptor alpha-subunit gene was measured in denervated chick skeletal muscle in response to calcium-active drugs, using a ribonuclease protection version of the conventional run-off assay. The L-channel agonist (-)Bay-K6844 and the calcium ionophore A23187 mimicked, and the intracellular chelator BAPTA and the calcium channel blockers D600 and nifedipine blocked, the effect of electrostimulation. These results suggest that influx of extracellular calcium is an integral component of the membrane depolarization-receptor gene inactivation cascade.
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PMID:Calcium influx blocks the skeletal muscle acetylcholine receptor alpha-subunit gene in vivo. 830 94