Actinomycin D inhibits the rapid increase in translatable calcitonin mRNA provoked by acute calcium stimulation
Autor: | Moukhtar Ms, N. Segond, Milhaud G, Stephane Minvielle, J. Taboulet, M.C. Delehaye, Jullienne A |
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Rok vydání: | 1989 |
Předmět: |
Calcitonin
Male medicine.medical_specialty Transcription Genetic Endocrinology Diabetes and Metabolism Clinical Biochemistry chemistry.chemical_element Gene Expression Stimulation Calcium Biology Biochemistry Cell-free system Endocrinology Internal medicine medicine Animals Secretion RNA Messenger Messenger RNA Biochemistry (medical) Thyroid Radioimmunoassay Rats Inbred Strains General Medicine Rats medicine.anatomical_structure chemistry Protein Biosynthesis Dactinomycin Hypercalcemia |
Zdroj: | Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 21(9) |
ISSN: | 0018-5043 |
Popis: | Calcium, injected to rats, elicits a rapid increase in translatable calcitonin mRNA, by acting probably at the post-transcriptional level, as no change in calcitonin mRNA could be detected by hybridization assay. In this study we have measured calcitonin mRNA extracted from rats subjected or not to acute hypercalcemia and pretreated or not with actinomycin D. Calcitonin mRNA was quantified by its ability to direct the synthesis of calcitonin (CT) precursors in a cell free system and by hybridization to a 32P cDNA probe specific for CT mRNA. Actinomycin D, injected 5 hours before calcium administration, decreased the incorporation of 3H adenine in liver and thyroid, but did not inhibit the rise in plasma levels of calcium and CT (measured by radioimmunoassay). The antibiotic was able to inhibit the eightfold increase in translatable mRNA elicited by calcium administration in the control animals. Hybridizable CT mRNA levels were not modified by the treatments. Thus the increase in translatable CT mRNA after calcium stimulation is independent of CT secretion and is probably due to post-transcriptional modifications involving the expression of other gene(s). |
Databáze: | OpenAIRE |
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