Disease relevance of Concentration Camps

• The binding of the Escherichia coli cyclic AMP receptor protein (CAP) to restriction fragments containing the lac promoter-operator region has been investigated as a function of cAMP concentration, using a sensitive gel electrophoresis assay [1].
• Renal cAMP concentration and renal prostaglandin (PG) E2 and PGF2alpha production were determined in control rats and rats with surgically induced myxedema [2].
• The signal for this acutely induced adaptation does not appear to be the decrease in cellular cAMP concentration resulting from inhibition of adenylate cyclase but does require a pertussis toxin-sensitive substrate [3].
• Changes in intracellular 3',5' cyclic AMP (cAMP) concentration regulate the development of natural competence in Haemophilus influenzae [4].
• Airway glands are defective in cystic fibrosis (CF), showing a complete absence of secretion to vasoactive intestinal peptide or forskolin, which increase intracellular cAMP concentration [5].

Psychiatry related information on Concentration Camps

• The Drosophila learning mutant rutabaga is defective in short-term memory and has a reduced intracellular cyclic adenosine monophosphate (cAMP) concentration [6].

High impact information on Concentration Camps

• The G protein-coupled, receptor-activated phosphoinositide 3-kinase gamma (PI3Kgamma) mediates inflammatory responses and negatively controls cardiac contractility by reducing cAMP concentration [7].
• We report that both adenylate cyclase activity and cAMP concentration increase substantially in induced neuroectoderm during neural induction [8].
• Many of these neuromodulators act via the intracellular second messenger cyclic AMP, but their effects on the spatial distribution of cAMP concentration have never been examined in an intact neural circuit [9].
• Additionally, ICV administration of leptin increased hypothalamic phosphatidylinositol 3-kinase (PI3K) and PDE3B activities and decreased cyclic AMP (cAMP) concentration [10].
• This mutation was shown to increase intracellular cAMP concentration and inhibit suppression of cAMP by adenosine [11].

Chemical compound and disease context of Concentration Camps

• While augmenting intracellular cAMP concentration, CT inhibits from 20 to 40% the generation of IL-1 activity from E. coli lipopolysaccharide (LPS)-stimulated adherent cells [12].
• These data indicate that GFAP expression is regulated by protein tyrosine phosphorylations, modulating the cAMP concentration and PI 3-K activity in C6 glioma cells [13].
• Nembutal reduced cellular cAMP concentration in colon cancer cells and resulted in a dose and time dependent decrease in MMP-2 and MMP-9 levels [14].

Biological context of Concentration Camps

• Concentrations of a type IV-specific phosphodiesterase inhibitor, rolipram, which had no significant effect on basal cAMP concentration, increased the cAMP response of hippocampal slices to stimulation with forskolin and induced persistent long-term potentiation in CA1 after a single tetanic train [15].
• E2 and 2-OHE2 had no effect, but 2-MeOE2 caused a significant (P < 0.05) increase in cAMP concentration in early S-phase and a decrease during mitosis [16].
• The remaining 28 single ligands produced changes in relatively few genes, even though they elicited measurable elevations in intracellular Ca(2+) and cAMP concentration and/or protein phosphorylation, including cytokines, chemokines, and other ligands that interact with G protein-coupled receptors [17].
• In a previous publication, we showed that VACs are rapidly exocytosed upon treatment with 8-Br-3',5'-cyclic adenosine monophosphate (8-Br-cAMP), a membrane-permeable analog of cAMP, and that this exocytosis correlates with variations in the cellular cAMP concentration in response to the cell-cell contacts [18].
• Using the stable cAMP derivative (8-(4-chlorophenylthio)-cAMP) as an inducer, we found that a 6-fold higher cAMP concentration was needed in HTC cells to achieve the same extent of enzyme induction as in Fu5-5 cells [19].

Anatomical context of Concentration Camps

• Dose-response curves for the local and distant effects of ISO and FSK on ICa were used as an index of cAMP concentration changes near the sarcolemma [20].
• To estimate the amplification of this step, we determined the cAMP concentration necessary to maximally inhibit superoxide anion production of formyl peptide-stimulated electropermeabilized cells, and we compare these concentrations to previously determined values of cAMP production in neutrophils [21].
• Subsequent treatment of mast cells with alpha-MSH increased the cAMP concentration in a characteristic biphasic pattern, demonstrating that alpha-MSH could affect intracellular processes [22].
• Oocytes treated with forskolin, an activator of adenylate cyclase, increase their cAMP concentration over 35-fold, up to 16 pmole cAMP/mg protein [23].
• The events that may take place during the prereplicative period and the antiproliferative effect of progesterone through a sustained increase in the cAMP concentration in the oviduct are discussed [24].

Associations of Concentration Camps with chemical compounds

• The greater response of cellular cAMP concentration to T3 and epinephrine when added together than to either agent added alone may explain their synergistic action to increase 2-DG uptake [25].
• Indomethacin (1 mM), when added alone, had no significant effect on short-circuit current (either basal or glucose-stimulated), Cl fluxes, or cAMP concentration [26].
• Indomethacin also inhibited the theophylline-evoked increase in cAMP concentration [26].
• After PGE2 and VIP, cAMP concentration increased, yet was likely independent of bicarbonate secretion [27].
• Two hour pretreatment with vinblastine also reduced by 40% the Isc response to the cholinergic agonist, carbamylcholine, a Ca-dependent secretory stimulus which does not increase cAMP concentration [28].

Gene context of Concentration Camps

• Although the heat shock element alone exhibits no UAS activity under conditions in which UASPDS promotes transcription, UASHS interacts positively with UASPDS to mediate high levels of SSA3 transcription in response to nutrient limitation and lowered intracellular cAMP concentration [29].
• In contrast, agents that increased cAMP concentration, abolished RPE proliferation, and MEK/ERK activation [30].
• Basal as well as GHRH-stimulated GTPase activity and intracellular cAMP concentration are also significantly greater in 293/G3R-4 cells as compared to 293/G5R-12 cells [31].
• This differential regulation of IFN-gamma and IL-10 expression was related to intracellular cAMP concentration [32].
• In strains carrying the cif1 mutation the intracellular concentration of ATP decreased immediately after addition of glucose while the intracellular concentration of cAMP did not increase. cAMP concentration increased in response to galactose or 2,4-dinitrophenol [33].

Analytical, diagnostic and therapeutic context of Concentration Camps

• The changes in cyclic AMP (cAMP) concentration and density of beta-adrenoceptors caused by electrical stimulation of the sympathetic innervation to parotid and submandibular glands of rat did not occur when the alpha- and beta-adrenergic antagonists, phentolamine, and propranolol were administered 20 min prior to initiation of stimulation [34].
• Corticosterone, pregnenolone concentrations in spent media, and the intracellular adenosine 3',5'-cyclic monophosphate (cAMP) concentration were determined by radioimmunoassay [35].
• In organ cultures of liver tissue from the axolotl, Ambystoma mexicanum, 1 nmol/l arginine vasotocin (AVT) increased tissue cyclic AMP (cAMP) concentration, activated glycogen phosphorylase, and caused glycogen breakdown and glucose release [36].
• In the control group the concentration of cAMP was 699 +/- 212 p.mol/g of wet tissue; carbachol administration resulted in an important and statistically significant increase (1030 +/- 205 p.mol/g; P less than 0.001) and isoprenaline increased the cAMP concentration more than twice (1414 +/- 368 p.mol/g, P less than 0.001) [37].
• The effect of vasopressin analogues on plasma adenosine 3',5'-cyclic monophosphate (cAMP) concentration was examined in a group of five conscious dogs instrumented for the measurement of arterial pressure and cardiac output (electromagnetic flowmeter) [38].

References