Disease relevance of N6-Monobutyryl-cAMP

• The data indicate that: (a) prostaglandin A1 is a very potent inhibitor of RNA synthesis in human chondrosarcomas; (b) N6-monobutyryladenosine 3',5'-cyclic monophosphate affects human chondrosarcomas differently than it does normal cartilage; and (c) responses of human chondrosarcomas to serum growth factors vary among individual tumors [1].
• N6-O'2-dibutyryl cAMP (dbcAMP), N6-monobutyryl cAMP (N6-mbcAMP), 8-Chloro cAMP (ClcAMP), and O'2-monobutyryl cAMP (O'2-mbcAMP) were used to study glial fibrillary acidic protein (GFAP) induction in rat C6 glioma [2].
• Arrhythmias could then be induced by subepicardial infusion (10 microliter/min) close to the visible edge of ischaemia of cAMP analogues [N6-monobutyryl cAMP, N6,O2'-dibutyryl cAMP (5.10(-2) M each)] or agents which increase the myocardial contents of cAMP [3].

High impact information on N6-Monobutyryl-cAMP

• N6-Monobutyryl-cAMP and 8-bromo-cAMP were equally potent in reducing IGF-II binding in the absence of insulin and inhibited maximal insulin-stimulated IGF-II binding by 60 and 30%, respectively [4].
• Moreover, when lipolysis was stimulated by the non-hydrolysable cAMP analogue N6-monobutyryl cAMP, bpV(pic), in contrast to insulin, maintained an antilipolytic effect [5].
• Vanadate, but not insulin, was also capable of increasing insulin binding as well as insulin sensitivity in insulin-resistant cells (treatment with N6-monobutyryl cAMP or amiloride and adipocytes from obese, aging rats) [6].
• Twenty-four hours after addition of 0.5 mM N6, O'2-dibutyryl cAMP (dbcAMP) or N6-monobutyryl cAMP (N6-mbcAMP) EC-SOD mRNA expression increased approximately twofold, while stimulation for 68 h with 0.5 mM N6-mbcAMP or 1 mM 8-Chloro cAMP (ClcAMP) and 1 mM dbcAMP enhanced the mean secreted activity/cell three- and fivefold, respectively [7].
• Administration of N6-monobutyryl cAMP iv (200 mg/kg/day) increased enzyme activity in normal (4.1 +/- 1.7 vs. 40.7 +/- 7.0 fmol/mg kidney.min) and phosphate-depleted mice (13.3 +/- 1.8 vs. 78.2 +/- 10.4) to a level significantly greater than that achieved in Hyp mice (7.4 +/- 1.1 vs. 22.7 +/- 3.6) [8].

Biological context of N6-Monobutyryl-cAMP

• Neither peroxovanadate nor insulin-inhibited lipolysis stimulated by N6-monobutyryl-cAMP, an analogue which is not hydrolysed by the cAMP-phosphodiesterase [9].
• Protein phosphorylation in human peripheral lymphocytes - stimulation by phytohemagglutinin and N6 monobutyryl cyclic AMP [10].
• On days 7 and 11 of pseudopregnancy, corpora lutea were obtained and incubated for 2 or 5 h in the presence of either 0.1 or 1 microgram/ml hCG or 1 mM monobutyryl cyclic AMP (bcAMP) [11].
• For analogs such as N6-benzoyl- and N6-monobutyryl-cAMP the method of determining I50 values provides information that is not obtainable by direct hydrolysis [12].

Anatomical context of N6-Monobutyryl-cAMP

• Further, the isolated poly A-containing RNA directs protein synthesis in an in vitro cell-free system, and stimulation of cartilage mRNA by N6-monobutyryl-cAMP does not alter the size distribution of the mRNA species synthesized from that present in control tissue [13].
• N6-Monobutyryl cAMP treated cartilage had an increased number of flattened immature chondrocytes with large nuclei and prominent nucleoli [14].
• The inhibitory potency of equimolar concentrations of cyclic adenosine monophosphate (cAMP) and three of its butyrylated derivatives; N6, O2'-dibutyryl cAMP (DBcAMP), N6-monobutyryl cAMP (N6MBcAMP) and O2' monobutyryl cAMP (O2' MBcAMP) was determined in isolated guinea pig ileal and aortic smooth muscle [15].
• In vitro organ culture of these pelvic cartilages in time-course experiments with N(6)-monobutyryl cyclic AMP (BtcAMP), insulin, and 5% rat serum demonstrated maximal stimulation of ODC activity between 4 and 6 h with each factor [16].

Associations of N6-Monobutyryl-cAMP with other chemical compounds

• (i) 8-Bromo cAMP and N6-monobutyryl cAMP but not dibutyryl cAMP are efficient cAMP analogs in Neurospora, stimulating mycelial elongation of the cr-1 mutants [17].
• Drugs that increase cyclic nucleotide levels in cells (cholera toxin, RO 20-1724, monobutyryl cyclic AMP, monobutyryl cyclic GMP) block the NAT decrease by light, whereas high potassium or EGTA do not block this light-induced NAT inactivation [18].
• Monobutyryl cyclic AMP and cyclic AMP increased the permeability to Na+ and Ca+ under conditions where no protein phosphorylation could occur [19].

Gene context of N6-Monobutyryl-cAMP

• These two antimetabolites, however, resulted in a slow but long-lived reversible suppression of corticosteroidogenesis in both ACTH- and monobutyryl cyclic AMP-stimulated, as well as unstimulated cultures of human cells [20].

Analytical, diagnostic and therapeutic context of N6-Monobutyryl-cAMP

• The present study assessed the specific effects of N6-monobutyryl-cAMP on RNA synthesis in the cartilage organ culture system [13].

References