• Korean Journal of Microbiology
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• v.24 no.2
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• pp.194-197
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• 1986

Malonate kinase and isocitrate lyase were induced in Acinetobacter calcoaceticus grown on malonate as a sole carbon source but repressed by succinate. The induction of those two enzymes was stimulated by dibutyryl cyclic adenosine 3', 5'-monophosphate, indicating that the expression of their genes for those enzymes is dependent on cyclic adenosine 3', 5'-monophosphate.

• Asian-Australasian Journal of Animal Sciences
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• v.1 no.3
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• pp.143-147
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• 1988

In order to investigate the mechanism of regulation of progesterone production, quail were hypophysectomized at various times during the ovulation cycle, and granulose cells were isolated from follicles 4 hr after the operation. They were incubated in vitro at $40^{\circ}C$ with or without LH or dibutyryl cyclic AMP, and the amounts of progesterone produced during 3 hr of incubation were measured by radioimmunoassay. Hypophysectomy at 8 hr or 20 hr before the predicted time of ovulation caused a reduced responsiveness of F1 granulosa cells to exogenous LH or dibutyrul cyclic AMP. Although hypophysectomy at 24 hr before ovulation caused a slight reduction of responsiveness of F1 granulosa cells, the reduction of the progesterone production during the incubation without any stimuli was prominent by the sham operation. These results suggest that the presence of pituitary gland influences the ability of the granulose cells to produce progesterone in response to LH or dibutyryl cyclic AMP.

• Animal cells and systems
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• v.9 no.3
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• pp.173-179
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• 2005

Cyclic-AMP-dependent protein kinase (PKA) seems to function as a negative regulator of the c-Jun $NH_2-terminal$ kinase (JNK) signaling pathway. We demonstrate here that the activity of the PKA catalytic subunit (PKAc) is reduced in apoptotic PC12 pheochromocytoma cells. Apoptotic progress was inhibited by dibutyryl cyclic AMP (dbcAMP), an analog of cAMP. The rescue by dbcAMP was attributable to inhibition of the JNK but not of the p38 signaling pathway, due to the induction of PKA activity. JNK was present in immunocomplexes of PKAc, and PKAc phosphorylated JNK in vitro. Presence of p38 kinase, however, was not prominent in immunocomplexes of PKAc. Our data suggest that JNK is a target point of negative regulation by PKAc in the JNK signaling pathway.

• The Korean Journal of Zoology
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• v.18 no.4
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• pp.221-229
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• 1975

The effect of adenosine 3', 5'-cyclic monophosphate on the ATPase activity and on the active transport of Ca of the sarcoplasmic reticulum fragments of the rabbit skeletal muscle was studied. Cyclic AMP (cAMP) had no effect on the ATPase activity of the fragments (8,000 ~ 20,000 $\times$ G and 20,000 ~ 36,000 $\times$ G fractions). $N^6$, O^{2'} -Dibutyryl cAMP (DBcAMP) had either no effect on the activity. On the other hand, theophylline (1 mM) increased the activity by about 20%. The active uptake of Ca by the sarcoplasmic reticulum fragments was inhibited by the presence of 1$\times$$10^{-6}$ ~ 1 $\times$ $10^{-3}$M of cAMP. The presence of DBcAMP or theophylline also inhibited the uptake. It is, therefore, concluded that the Ca uptake of the sarcoplasmic reticulum seems to be controlled by cAMP.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.30 no.4
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• pp.37-48
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• 2017

Objectives : This Study was conducted to investigate the melanin synthesis effect of Eclipta prostrata and to determine the relationship between melanin synthesis effect of Eclipta prostrata and cAMP/PKA melanin synthesis pathway. Methods : We measured melanin contents, tyrosinase activity, expression of TRPs, p-CREB in B16F10 cells cultured with Eclipta prostrata ethanol extracts(EEP). And after treatment with H89 and dibutyryl cAMP, which inhibit or promote the activation of PKA, we observed changes in melanin synthesis and tyrosinase activity stimulated by EEP. Results : EEP increased melanin synthesis by promoting the expression of tyrosinase and TRP-1. It also promoted expression of p-CREB. H89 suppresses melanogenic effect and expression of tyrosinase, TRP-1 in B16F10 stimulated by EEP. Dibutyryl cAMP promotes melanogenic effect of EEP. Conclusions : The results of this study suggest that melanin synthesis effect of EEP is related to induction of tyrosinase and TRP-1 expression through the cAMP/PKA pathway.

• Herbal Formula Science
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• v.28 no.1
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• pp.81-90
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• 2020

Objectives : This study was conducted to investigate the effects of major constituents of Epimedium koreanum Nakai (Icariin, epimedium A, epimedium B, and epimedium C) on melanin synthesis. Methods : We measured melanin contents, tyrosinase activity, and expression of Rab27a in B16F10 cells cultured with Epimedium koreanum Nakai ethanol extract (EKN) and their major constituents. After treatment with H89 and dibutyryl cAMP, which inhibit or promote the activation of PKA, we observed changes in melanin synthesis and tyrosinase activity stimulated by EKN. Results : Among them, EKN and icariin enhanced tyrosinase activity and melanin contents. We confirmed that EKN augmented melanin synthesis via cAMP/PKA pathway. Icariin-induced tyrosinase activity and melanin content were attenuated by PKA inhibitor H89, while melanogenic effect of icariin was further augmented by cAMP analog, dbc AMP. However, icariin did not affect the expression of small GTPase Rab27a involved in melanosome transport. Conclusions : These results suggest that icariin promotes melanogenesis through cAMP/PKA pathway but does not affect small GTPase Rab27a.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.6
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• pp.333-339
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• 2005

B/K protein is a novel protein containing double C2-like domains. We examined the specific signaling pathway that regulates the transcription of B/K in PC12 cells. When the cells were treated with forskolin ($50{\mu}M$), B/K mRNA and protein levels were time-dependently decreased, reaching the lowest level at 3 or 4 hr, and thereafter returning to the control level. Chemicals such as dibutyryl-cAMP, cellpermeable cyclic AMP (cAMP) analogue and CGS21680, adenosine receptor $A_{2A}$ agonist, also repressed the B/K transcription. However, 1,9-dideoxyforskolin did not show inhibitory effect on B/K transcription, suggesting direct involvement of cAMP in the forskolin-induced inhibition of B/K transcription. Effect of forskolin, dibutyryl cAMP and CGS21680 was significantly reduced in PKA-deficient PC12 cell line (PC12-123.7). One cAMP-response element (CRE)-like sequence (B/K CLS) was found in the promoter region of B/K DNA, and electrophoretic mobility shift assay indicated its binding to CREM and CREB. Forskolin significantly suppressed the promoter activity in CHO-K1 cells transfected with the constructs containing B/K CLS, but not with the construct in which B/K CLS was mutated (AC：TG). Taken together, we suggest that the transcription of B/K gene in PC12 cells may be regulated by PKA-dependent mechanism.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.1
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• pp.97-105
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• 1997

The regulatory role of cyclic nucleotides in the expression of neutrophil responses has been examined. fMLP-stimulated superoxide production in neutrophils was inhibited by dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), histamine, adenosine + theophylline, cAMP elevating agents, and 8-bromoguanosine 3' ,5' -cyclic monophosphate (8-BrcGMP) and sodium nitroprusside, cGMP elevating agents. Staurosporine, a protein kinase C inhibitor, genistein, a protein tyrosine kinase inhibitor and chlorpromazine, a calmodulin inhibitor, inhibited superoxide production by fMLP, but they did not further affect the action of DBcAMP on the stimulatory action of fMLP. DBcAMP, histamine, adenosine+theophylline and genistein inhibited myeloperoxidease release evoked by fMLP, whereas BrcGMP, sodium nitroprusside and staurosporine did not affect it. The elevation of $[Ca^{2+}]_i$ evoked by fMLP was inhibited by genistein and chlorpromazine but was not affected by staurosporine. DBcAMP exerted little effect on the initial peak in $[Ca^{2+}]_i$ response to fMLP but effectively inhibited the sustained rise. On the other hand, BrcGMP significantly inhibited both phases. fMLP-induced $Mn^{2+}$ influx was inhibited by either DBcAMP or BrcGMP. These results suggest that fMLP-stimulated neutrophil responses may be regulated by cAMP more than cGMP. cAMP and cGMP appear not affect stimulated responses by direct protein kinase C activation. Their regulatory action on the stimulated neutrophil responses may be not influenced by other activation processes.

• Applied Microscopy
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• v.7 no.1
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• pp.21-43
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• 1977

This experiment was undertaken in order to localize the labeled dbcAMP (dibutyryl cyclic AMP) in oocytes whose development has been suppressed by cold dbcAMP for 6 or 19 hours in vitro. Mouse oocytes were obtained from the ovaries of 3-4 week old A strain female mice, by puncturing the Graafian follicles in the modified Krebs-Ringer bicarbonate salt solution under the dissecting microscope. Those oocytes which have intact germinal vesicle were cultured in the basic culture medium supplemented with 0.4% bovine serum albumin (BSA). Cultivation of the oocytes was carried out in a microtube developed by Cho (1974). The cultures were then incubated in a humidified 5% $CO_2$ incubator maintained at $37^{\circ}C$ for 6 or 19 hours (Donahue, 1968). DbcAMP was added to culture medium for a final concentration of 100ug/ml, and $^3H-dbc$ AMP (specific activity 13 Ci/mM) for a final concentration of $40{\mu}Ci/ml$ was also added to the medium. For electron microscopic autoradiography, those oocytes recovered from the culture were washed with phosphate buffer (pH 7.4), and immediately prefixed in a 2.5% glutaraldehyde overnight and postfixed for 2 hours at $4 ^{\circ}C$ in 1% osmium tetroxide in phosphate buffer with pH 7.4 (Palade, 1952). After fixation, the materials were dehydrated in graded alcohol series and embedded in Epon 812 mixture based on the standard procedures (Luft, 1961). The thin sections $600-700{\AA}$ thick were mounted on the grids of 200 meshes. The grids containing sections were coated with a nuclear emulsion Kodak NTB-3 and stored in a cold dark box (at $4^{\circ}C$) for 3 weeks. After exposure, the samples were developed with Kodak D-19 and stained with uranyl acetate and lead citrate. Routine observation was made with Hitachi HU-11E electron microsocope. The results of the observation were as followings: 1. It was found that the labeled dbcAMP penetrated the egg plasma membrane and dispersed at random in the cytoplasm. 2. It was also observed that most of the labeled dbcAMP was attached to microfibrillar lattices portion of the oocyte cytoplasm. There fore, it is presumed that the receptor of the dbcAMP is localized in the microfibrillar lattices of the oocyte. 3. It also seems that some other cell organells such as mitochondria, Golgi complex, cortical granules are not directly related to the action of the dbcAMP. 4. The labeled dbcAMP was neither observed in the membrane nor in the nucleus. Therefore, it seems that there is no relationship between the concentration of dbcAMP and the nuclear membranous permeability. 5. There was no difference in number of dbcAMP particles when oocytes were cultured for 6 hours and 19 hours. 6. However, it was observed that, in same of the oocytes suppressed in germinal vesicle by dbcAMP for 19 hours, cell organells were moved and concentrated to a small portion of the cytoplasm, and that the morphology of the organells greatly changed to an abnormal. form. Therefore, it is supposed that those oocytes were in the process of degeneration. From the above results, it is expected that dbcAMP penetrated the egg membrane and was bound to the receptor which seems to be located in the microfibrillar lattiees portion, and that this dbcAMP-receptor complex inhibited some enzyme system of the oocytes which are essential for the germinal vesicle breakdown.

• BMB Reports
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• v.42 no.10
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• pp.642-647
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• 2009

In this study, the effects of $Ca^{2+}$ and cyclic adenosine monophosphate (cAMP) on microsomal triglyceride (TG) transfer protein (MTP) activity were investigated in rat liver. MTP activity was high when liver contained low levels of cAMP, which was induced by administration of glucose, or high levels of total $Ca^{2+}$ and TG. However, MTP activity increased by high levels of $Ca^{2+}$ and TG was reduced in a dose-dependent manner by treatment with dibutyryl-cAMP (db-cAMP), a cAMP analogue. Conversely, when homogenates of liver from normal rats, with low levels of total $Ca^{2+}$ and high levels of cAMP, were incubated with thapsigargin, a $Ca^{2+}$-inducer, MTP activity was increased in a dose-dependent manner compared to control. Therefore, our results suggest that high levels of $Ca^{2+}$ cause hypertriglyceridemia through the elevation of MTP activity, as opposed to high levels of cAMP, which suppress MTP activity and inhibit hypertriglyceridemia.