Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study is to characterize the adenyl cyclase (AC) activity in Fisher rat thyroid cell line when stimulated with several agonists, such as: forskolin, sodium fluoride, Gpp(NH)p (guanosine-5'-(beta, gamma -imino) triphosphate or thyrotropin. The following studies such as: dose-response, pH, temperature, time-response, millieu concentration, 3H-thymidine uptake, Km and Vm study were also performed. Adenyl cyclase activity was measured as adenosine 3', 5'-cyclic monophosphate generated by cell cultures in 120- minutes incubation at 37 degrees C. The basal AC activity was 15.0 +/- 7.0 (mean +/- SEM, n = 6) pmol/100,000 cells/120 minutes. Forskolin at 0.1 mM increased the AC activity to 10 folds of basal AC activity. Thyroid stimulating hormone at 1 mU/ml and 10 mU/ml increased the AC activity 2 and 15 folds, respectively. Sodium fluoride stimulation study demonstrated dual actions of fluoride on adenylate cyclase; when the cells were assayed with increasing concentration of NaF, the AC activity increased as the concentration of NaF increased from 0.01 to 1 mM, but decreased strikingly as that concentration increased from 1 mM to 100 mM. When the concentration of nonhydrolyzable guanine nucleotide analogs increased in the presence of TSH, there was first an increase in adenylate cyclase activity, followed by a decrease at higher concentration. The amount of cAMP generation was much higher (P < 0.05) in hypotonic than in isotonic millieu. When the incubation temperature raised to 56 degrees C, all the AC activity was diminished. The optimal pH for AC activity was in the range of 7.4 and 8.0.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The characterization of adenyl cyclase activity in FRTL-5 cell line. 838 68

The role of guanine nucleotide binding protein in phosphoinositide metabolism in the central nervous system was studied in rat brain cortical slices prelabelled with [(3)H]inositol. Addition of guanosine triphosphate and its analogs increased the accumulation of [(3)H]inositol monophosphate in the presence of lithium chloride (10 mM). These stimulatory effects were specific for the guanine moiety as no measurable effect was observed with other adenine nucleotides. Forskolin and dibutyryl cyclic adenosine monophosphate did not affect the phosphoinositide hydrolysis, indicating that the guanine nucleotide effect on phosphoinositide hydrolysis is not mediated by the activation of the adenylate cyclase system. Sodium fluoride, a direct activator of guanine nucleotide binding protein, also increased the accumulation of [(3)H]inositol monophosphate in a concentration-dependent manner, and the observed effect was specific for fluoride ion. Taken together, the results support and extend earlier suggestions that a putative guanine nucleotide binding protein is involved in phosphoinositide metabolism in the central nervous system.
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PMID:Activation of phosphoinositide hydrolysis in rat cortical slices by guanine nucleotides and sodium fluoride. 2050 97


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