• Journal of Life Science
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• v.10 no.3
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• pp.279-285
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• 2000

CRP (cyclic AMP receptor protein) regulate transcription of catabolite-sensitive genes in Escherichia coli. Wild-type and mutant CRP (S83G and S128A) proteins were used to measure the thermal stability and the temperature-dependent structural change by proteolytic digestion, UV spectrophotometer and CD spectrapolarimeter. The result indicated that wild-type CRP was more thermally stable than the mutant CRPs in the presence of cAMP. At a low temperature, wild-type CRP with cAMP was more sensitive to subtilisin than the mutant CRPs. At a high temperature, there was no difference of sensitivity to subtilisin among wild-type, S83G and S128A CRPs. CD spectra suggested that the secondary structure of CRP was destroyed partially at a high temperature.

• Microbiology and Biotechnology Letters
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• v.34 no.4
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• pp.289-298
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• 2006

3',5'-cyclic adenosine monophosphate (cAMP) is an important molecule, which mediates diverse cellular processes. For example, it is involved in regulation of sugar uptake/catabolism, DNA replication, cell division, and motility in various acterial species. In addition, cAMP is one of the critical regulators for syntheses of virulence factors in many pathogenic bacteria. It is believed that cAMP acts as a signal for environmental changes as well as a regulatory factor for gene expressions. Therefore, intracellular concentration of cAMP is finely modulated by according to its rates of synthesis (by adenylate cyclase), excretion, and degradation (by cAMP phosphodiesterase). In the present review, we discuss the bacterial physiological characteristics governed by CAMP and the molecular mechanisms for gene regulation by cAMP. Furthermore, the effect of cAMP on phosphotransferase system is addressed.

• Journal of Ginseng Research
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• v.12 no.2
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• pp.135-144
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• 1988

When ginseng saponin fractions were treated with secretion regulatory agents, it increased cAMP level at the case of thyrotropin (but the amounts were small). Total saponin increased cAMP level at DEcAMP and isoproterenol, and decreased the level at carbachol and propranolol, but at NaF it had little effect. When diol saponin or triol saponin were treated with secretion regulatory agents, biol saponin decreased cAMP level but triol saponin increased it except for isoproterenol. Also, in propra%olol, which inhibits the increase of CAMP level, diol and triol saponin showed crossing effect, too. From the above results, ginseng saponin fractions are believed that it has the, effects of promotion or inhibition on cAMP production in the thyroid , both diol saponin and triol saponin have crossing effect on thyroid hormone secretion regulatory agents. The normalizatin action of ginseng saponin fractions is notable at the case of NaF and carbachol.

• YAKHAK HOEJI
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• v.47 no.1
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• pp.31-36
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• 2003

To investigate the effect of protein kinase on melanin production via cAMP-dependent pathway, we measured the melanin amount and tyrosinase activity in B16 melanoma cells stimulated by alpha-melanocyte stimulating hormone (MSH), forskolin and 8-Br-cAMP. MSH, forskolin and 8-Br-cAMP significantly increased both melanin production and tyrosinase activity in B16 cells. Melanin production and tyrosinase activity by MSH are significantly inhibited by cyclic AMP-dependent protein kinase inhibitor (KT5720) and protein kinase C down-regulation treated with PMA. Bisindolmaleimide (1$\mu$M), protein kinase C inhibitor, significantly inhibited melanin production and tyrosinase activity stimulated by MSH, forskolin and 8-Br-cAMP with the following order of potency: MSH＞forskolin＞8-Br-cAMP. Tyrosine kinase inhibitor, genistein and DHC, significantly inhibited both, but the inhibitory effect was more potent in 8-Br-cAMP-stimulated B16 cells than MSH-stimulated cells. NFkB inhibitor (parthenolide) significantly inhibited melanin production and tyrosinase activity. Neither melanin production nor tyrosinase activity induced by MSH, forskolin and 8-Br-cAMP were affected by KN-62 (calmodulin-dependent protein kinase II inhibitor), PD098059 (mitogen-activated protein kinase inhibitor, MAPKK) and worthmannin (phosphatidylinositol 3-kinase inhibitor). These results suggest that both protein kinase C and tyrosine kinase are involved in melanin production by cyclic AMP-dependent pathway and NFkB pathway may play an important role in cyclic AMP-dependent melanin production in B16 melanoma cells.

• Bulletin of the Korean Chemical Society
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• v.31 no.2
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• pp.442-446
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• 2010

Adenosine 3',5'-cyclic monophosphate (cAMP) is a second messenger responsible for a multitude of cellular responses. In this study, we utilized $\beta$-cyclodextrin ($\beta$-CD) as an artificial receptor with a hydrophobic cavity to elucidate the inclusion kinetics of cAMP in a hydrophobic environment using the ultrasonic relaxation method. The results revealed that the interaction of cAMP with $\beta$-CD followed a single relaxation curve as a result of host-guest interactions. The inclusion of cAMP into the $\beta$-CD cavity was found to be a diffusion-controlled reaction. The dissociation of cAMP from the $\beta$-CD cavity was slower than that of adenosine 5'-monophosphate (AMP). The syn and anti glycosyl conformations of adenine nucleotides are considered to play an important role in formation of the inclusion complex. Taken together, our findings indicate that hydrophobic interactions are involved in the inclusion complex formation of cAMP with $\beta$-CD and provide insight into the interactions of cAMP with cAMP-binding proteins.

• Animal cells and systems
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• v.11 no.2
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• pp.169-173
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• 2007

Hyperpolarization-activated nonselective cation channels (HCNs) play a pivotal role in producing rhythmic electrical activity in the heart and the nerve cells. In our previous experiments, voltage-dependent $Cd^{2+}$ access to one of the substituted cysteines in S6, T464C, supports the existence of an intracellular voltage-dependent activation gate. Direct binding of intracellular cAMP to HCN channels also modulates gating. Here we attempted to locate the cAMP-modulated structure that can modify the gating of HCN channels. SpHCN channels, a sea urchin homologue of the HCN family, became inactivated rapidly and intracellular cAMP removed this inactivation, resulting in about eight-fold increase of steady-state current level. T464C was probed with $Cd^{2+}$ applied to the intracellular side of the channel. We found that access of $Cd^{2+}$ to T464C was strongly gated by cAMP as well as voltage. Release of bound $Cd^{2+}$ by DMPS was also gated in a cAMP-dependent manner. Our results suggest the existence of an intracellular cAMP-modulated gate in the lower S6 region of spHCN channels.

• Journal of Ginseng Research
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• v.21 no.3
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• pp.141-146
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• 1997

The role of cAMP in the differentiation process of F9 cells induced by ginsenosides was examined by performing transient transfixion assay with CRE-luciferase reporter plasmid, GR thansactivation assay with GRE-luciferase activity with or without treatment of CAMP and forskolin, an activator of adenylate cyclase, and protein klnase A assay in the presence of ginsenosides. Ginsenosides had no effect on CRE-transactivation activity, whereas retinoic acid induced the activity. When cAMP or forskolin was treated with ginsenosides, GRE-luciferase activity was further augumented by them. In addition, ginsenosides induced protein kinase A activity in the presence of cAMP. These results suggest that ginsenosides activate cAMP-dependent protein kinase A which, in turn, increase GR activity in F9 cells.

• Journal of Microbiology and Biotechnology
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• v.19 no.12
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• pp.1527-1535
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• 2009

Polyphosphate (polyP) plays diverse physiological functions in prokaryotes and eukaryotes, but most of their detailed mechanisms are still obscure. Here, we show that deletion of polyphosphate kinase (PPK), the principal enzyme responsible for synthesis of polyP, resulted in augmented expression of cAMP receptor protein (CRP) and rpoS and lowered $H_2O_2$ sensitivity in Salmonella Typhimurium ATCC14028. The binding of cAMP-CRP complex to rpoS promoter and further stimulation of its transcription were proved through electrophoretic mobility shift assay, lacZ fusion, and exogenous cAMP addition, respectively. The rpoS expression increased in cpdA (cAMP phosphodiesterase coding gene) mutant, further suggesting that cAMP-CRP upregulated rpoS expression. These results demonstrate that PPK affects oxidative stress response by modulating crp and rpoS expression in S. Typhimurium.

• BMB Reports
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• v.30 no.5
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• pp.320-325
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• 1997

Thioredoxin is a multi-functional protein which is ubiquitous in microorganisms, animals and plants. Previously, expression of the E. coli thioredoxin gene was found to be negatively regulated by cAMP. In the present study, the effect of cAMP on two separate promoters of the E. coli thioredoxin gene was investigated. Cyclic AMP had a repressible effect on P1 and P1P2 promoter activity of the constructs. This effect was also observed in the cya strain. The P2 promoter construct gave very high -galactosidase activity, and its expression was not affected by exogenous cAMP. It was assumed that a cis-acting negative element, probably the cAMP-CRP binding site, might have been deleted in the P1 promoter construct. Repression of the thioredoxin gene expression by cAMP appeared to be independent of ppGpp.

• The korean journal of orthodontics
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• v.16 no.1
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• pp.51-70
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• 1986

Parathyroid hormone (PTH) is known to exert its effects on bone cells through the mediation of adenosine 3', 5'-monophosphate (cAMP). Orthodontic forces have also been shown to alter the cAMP content of paradental cells, particularly the alveolar bone osteoblasts. The objective of this experiment was to determine whether a combined orthodontic treatment-PTH administration regimen would have an additive effect on cAMP content in paradental cells in sites of periodontal ligament (PDL) tension. Seven groups of 4 one year old female cats each were treated for 1,3,6,12,24 h, 7 and 14 d by tipping one maxillary canine. PTH was administered twice daily, 30u/kg. Maxillary horizontal sections were stained immunohistochemically for cAMP and the degree of cellular staining intensity was determined microphotometrically as per cent light transmittance at 600nm. Alveolar bone osteoblasts, progenitor cells, PDL fibroblasts and cementoblasts in tenion sites were measured and the data were analyzed statistically by a mixed model analysis of variance. PTH administration increased the cAMP staining of nonorthodontically treated paradental cells in comparison to cells untreated by force or hormone. Cells in PDL tension sites of PTH-treated cats demonstrated significantly darker cAMP staining than cells in non-orthodontically-treated sites. Osteoblasts demonstrated the greatest response in terms of cAMP elevation, while in PDL fibroblasts orthodontic force did not increase cAMP levels above those measured in non-stretched hormonally-treated cells. These results demonstrate that PTH increases cAMP levels in paradental cells, particullarly in osteoblasts, and that the effects of PTH and orthodontic forces on paradental target cells may approach additivity.