Cyclic CMP
2',3'-Cyclic Nucleotide 3'-Phosphodiesterase
Cytidine Monophosphate
Fetal Alcohol Spectrum Disorders
Infant Behavior
Alcohol Drinking
Ethanol
Pregnancy
Suppression of hypoxia-associated vascular endothelial growth factor gene expression by nitric oxide via cGMP. (1/43)
PURPOSE: To investigate the suppressive effect of nitric oxide (NO) on vascular endothelial growth factor (VEGF) gene expression and to elucidate its mechanism of action. METHODS: Immortalized human retinal epithelial (RPE) cells, H-ras-transfected murine capillary endothelial cells, and nuclear factor-kappaB (NF-kappaB) RelA knockout 3T3 fibroblasts had VEGF gene expression stimulated by hypoxia, TPA (phorbol ester 12-O-tetradecanoylphorbol-13 acetate), and ras-transfection. The dose response and time course of inhibition of VEGF gene expression by NO were characterized by northern blot analysis, ribonuclease protection assay, and enzyme-linked immunosorbent assay. The effects of NF-kappaB and cGMP in the NO-induced suppression of VEGF gene expression were quantitated. cGMP production was inhibited by LY 83583 (6-anilino-5,8-quinolinedione), a specific inhibitor of guanylate cyclase production, and cGMP accumulation was quantitated by immunoassay. RelA knockout 3T3 fibroblasts were used to assess the contribution of NF-kappaB to the downregulation of VEGF by NO. RESULTS: The NO donor sodium nitroprusside (SNP) decreased hypoxia-induced VEGF gene expression in a dose- and time-dependent manner. One hundred fifty micromolar SNP completely suppressed hypoxia-induced VEGF mRNA levels for at least 24 hours. Constitutive VEGF expression was not altered by SNP. The SNP-mediated decreases in VEGF expression were associated with increases in intracellular cGMP and were blocked by LY 83583. Sodium nitroprusside was able to decrease hypoxia-induced VEGF mRNA increases in fibroblasts deficient in the RelA subunit of NF-kappaB. Nitric oxide was also effective at suppressing increased VEGF expression secondan, to mutant ras and TPA. CONCLUSIONS: These data indicate that NO decreases hypoxia-induced VEGF via a cGMP-dependent mechanism and suggest that NO may serve as an endogenous inhibitor of both hypoxia- and non- hypoxia-enhanced VEGF expression in vivo. (+info)Generating new ligand-binding RNAs by affinity maturation and disintegration of allosteric ribozymes. (2/43)
Allosteric ribozymes are engineered RNAs that operate as molecular switches whose rates of catalytic activity are modulated by the binding of specific effector molecules. New RNA molecular switches can be created by using "allosteric selection," a molecular engineering process that combines modular rational design and in vitro evolution strategies. In this report, we describe the characterization of 3',5'-cyclic nucleotide monophosphate (cNMP)-dependent hammerhead ribozymes that were created using allosteric selection (Koizumi et al., Nat Struct Biol, 1999, 6:1062-1071). Artificial phylogeny data generated by random mutagenesis and reselection of existing cGMP-, cCMP-, and cAMP-dependent ribozymes indicate that each is comprised of distinct effector-binding and catalytic domains. In addition, patterns of nucleotide covariation and direct mutational analysis both support distinct secondary-structure organizations for the effector-binding domains. Guided by these structural models, we were able to disintegrate each allosteric ribozyme into separate ligand-binding and catalytic modules. Examinations of the independent effector-binding domains reveal that each retains its corresponding cNMP-binding function. These results validate the use of allosteric selection and modular engineering as a means of simultaneously generating new nucleic acid structures that selectively bind ligands. Furthermore, we demonstrate that the binding affinity of an allosteric ribozyme can be improved through random mutagenesis and allosteric selection under conditions that favor tighter binding. This "affinity maturation" effect is expected to be a valuable attribute of allosteric selection as future endeavors seek to apply engineered allosteric ribozymes as biosensor components and as controllable genetic switches. (+info)Phenanthrolines--a new class of CFTR chloride channel openers. (3/43)
1. A number of phenanthrolines and benzoquinolines were examined for their ability to activate epithelial chloride secretion by measuring short circuit current (SCC) using the mouse colon epithelium. 1,10 phenanthroline stimulated electrogenic chloride secretion with an EC(50) of 612+/-10 microM and a Hill slope of 4.9+/-0.3. A similar pharmacology was demonstrated by both 1,7 and 4,7 phenanthrolines, 7,8 benzoquinoline and phenanthridine. 2. Evidence that the increase in SCC caused by 1,10 phenanthroline was due to chloride secretion is based upon (a) inhibition of the current by furosemide, (b) failure of cystic fibrosis (CF) colons to respond and (c) an associated net flux of (36)Cl(-). 3. 1,10 Phenanthroline affected neither the generation of cyclic AMP or the concentration of intracellular Ca(2+) in colonic epithelial cells. 4. 1,10 phenanthroline affected the chloride conductance of the apical membrane, as shown by an increase in chloride current in 'apical membrane only' preparations in the presence of an apical to basolateral chloride gradient. The increase in chloride current was inhibited by 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and was not present in CF colons. 5. Additionally, 1,10 phenanthroline activated basolateral K(+) channels, both Ca(2+)- and cyclic AMP-sensitive channels, as shown by inhibitor studies with charybdotoxin (ChTX) and XE991, and after the apical membrane was permeabilized with nystatin. 6. The phenanthrolines and benzoquinolines described here, with dual actions affecting CFTR and basolateral K(+) channels, may constitute useful lead compounds for adjunct therapy in CF. (+info)Contribution of Gln9 and Phe80 to substrate binding in ribonuclease MC1 from bitter gourd seeds. (4/43)
Ribonuclease MC1 (RNase MC1) isolated from bitter gourd (Momordica charantia) seeds specifically cleaves phosphodiester bonds on the 5'-side of uridine. The crystal structures of RNase MC1 in complex with 2'-UMP or 3'-UMP reveal that Gln9, Asn71, Leu73, and Phe80 are involved in uridine binding by hydrogen bonding and hydrophobic interactions [Suzuki et al. (2000) Biochem. Biophys. Res. Commun. 275, 572-576]. To evaluate the contribution of Gln9 and Phe80 to uridine binding, Gln9 was replaced with Ala, Phe, Glu, or His, and Phe80 with Ala by site-directed mutagenesis. The kinetic properties of the resulting mutant enzymes were characterized using cytidylyl-3',5'-uridine (CpU) as a substrate. The mutant Q9A exhibited a 3.7-fold increased K(m) and 27.6-fold decreased k(cat), while three other mutations, Q9F, Q9E, and Q9H, predominantly affected the k(cat) value. Replacing Phe80 with Ala drastically reduced the catalytic efficiency (k(cat)/K(m)) with a minimum K(m) value equal to 8 mM. It was further found that the hydrolytic activities of the mutants toward cytidine-2',3'-cyclic monophosphate (cCMP) were reduced. These results demonstrate that Gln9 and Phe80 play essential roles not only in uridine binding but also in hydrolytic activity. Moreover, we produced double Ala substituted mutants at Gln9, Asn71, Leu73, and Phe80, and compared their kinetic properties with those of the corresponding single mutants. The results suggest that these four residues may contribute to uridine binding in a mutually independent manner. (+info)The HD domain of the Escherichia coli tRNA nucleotidyltransferase has 2',3'-cyclic phosphodiesterase, 2'-nucleotidase, and phosphatase activities. (5/43)
In all mature tRNAs, the 3'-terminal CCA sequence is synthesized or repaired by a template-independent nucleotidyltransferase (ATP(CTP):tRNA nucleotidyltransferase; EC 2.7.7.25). The Escherichia coli enzyme comprises two domains: an N-terminal domain containing the nucleotidyltransferase activity and an uncharacterized C-terminal HD domain. The HD motif defines a superfamily of metal-dependent phosphohydrolases that includes a variety of uncharacterized proteins and domains associated with nucleotidyltransferases and helicases from bacteria, archaea, and eukaryotes. The C-terminal HD domain in E. coli tRNA nucleotidyltransferase demonstrated Ni(2+)-dependent phosphatase activity toward pyrophosphate, canonical 5'-nucleoside tri- and diphosphates, NADP, and 2'-AMP. Assays with phosphodiesterase substrates revealed surprising metal-independent phosphodiesterase activity toward 2',3'-cAMP, -cGMP, and -cCMP. Without metal or in the presence of Mg(2+), the tRNA nucleotidyltransferase hydrolyzed 2',3'-cyclic substrates with the formation of 2'-nucleotides, whereas in the presence of Ni(2+), the protein also produced some 3'-nucleotides. Mutations at the conserved His-255 and Asp-256 residues comprising the C-terminal HD domain of this protein inactivated both phosphodiesterase and phosphatase activities, indicating that these activities are associated with the HD domain. Low concentrations of the E. coli tRNA (10 nm) had a strong inhibiting effect on both phosphatase and phosphodiesterase activities. The competitive character of inhibition by tRNA suggests that it might be a natural substrate for these activities. This inhibition was completely abolished by the addition of Mg(2+), Mn(2+), or Ca(2+), but not Ni(2+). The data suggest that the phosphohydrolase activities of the HD domain of the E. coli tRNA nucleotidyltransferase are involved in the repair of the 3'-CCA end of tRNA. (+info)Cofactor fingerprinting with STD NMR to characterize proteins of unknown function: identification of a rare cCMP cofactor preference. (6/43)
Proteomics efforts have created a need for better strategies to functionally categorize newly discovered proteins. To this end, we have employed saturation transfer difference NMR with pools of closely related cofactors, to determine cofactor preferences. This approach works well for dehydrogenases and has also been applied to cyclic nucleotide-binding proteins. In the latter application, a protein (radial spoke protein-2, RSP2) that plays a central role in forming the radial spoke of Chlamydomonas reinhardtii flagella was shown to bind cCMP. cCMP-binding proteins are rare, although previous reports of their presence in sperm and flagella suggest that cCMP may have a more general role in flagellar function. 31P NMR was used to monitor the preferential hydrolysis of ATP versus GTP, suggesting that RSP2 is a kinase. (+info)Hypertonicity regulates the aquaporin-2 promoter independently of arginine vasopressin. (7/43)
BACKGROUND: Aquaporin-2 (AQP-2) is an arginine vasopressin (AVP)-regulated water channel in kidney collecting duct cells. The present study was undertaken to determine whether a change in tonicity could directly regulate the AQP-2 gene in an in vitro experiment. METHODS: Various fragments of the 5'-flanking region of the murine AQP-2 gene up to -9.5 kb were cloned into a luciferase (Luc) reporter plasmid, and they were transiently transfected into Madin-Darby canine kidney cells. RESULTS: Hypertonicity significantly increased the Luc activity of the constructs containing >6.1 kb of the 5'-flanking region of the AQP-2 gene (-6.1AQP2). However, promoter regions <4.3 kb in length containing the tonicity-responsive enhancer (TonE) at bp -570 to -560 were not stimulated by hypertonicity. The TonE-deleted construct which contains -9.5 to -1.1 kb of the 5' side of the AQP-2 gene, 8.4AQP2, was also stimulated by hypertonicity. Mitogen-activated protein (MAP) kinase inhibitors SB203580 and U0126 did not affect the Luc activity of -6.1AQP2 induced by hypertonicity. In addition, the vector expressing dominant-negative TonE-binding protein (TonEBP) did not affect the hypertonicity-induced Luc activity of -6.1AQP2. The Luc activity of -6.1AQP2 was stimulated by the overexpression of TonEBP. Hypertonicity further increased the Luc activity of -6.1AQP2 under the overexpression of TonEBP. CONCLUSION: These findings indicate that hypertonicity regulates AQP-2 promoter activity via an AVP-independent mechanism, and that the tonicity-responsive element resides between the -6.1 and -4.3 kb 5'-flanking region of the AQP-2 gene, in which the structure and mechanism of response to hypertonicity could be distinct from those of TonE. (+info)A comparison of the diagnostic accuracy and prognostic value of the first and second anti-cyclic citrullinated peptides (CCP1 and CCP2) autoantibody tests for rheumatoid arthritis. (8/43)
OBJECTIVES: To compare the diagnostic performance and prognostic value of the anti-cyclic citrullinated peptide (CCP1) and anti-CCP2 autoantibody tests in a clinical setting. METHODS: Anti-CCP1 and anti-CCP2 antibody tests were performed on the same serum samples obtained from 467 patients with early arthritis from the Leiden Arthritis Cohort. The sensitivity, specificity, positive predictive value, and negative predictive value for discriminating between rheumatoid arthritis (RA) and non-RA at 1 year's follow up were calculated for both tests. Results were graphically presented using receiver operating characteristic curves. Progression of radiological joint damage was assessed over 4 years in patients with RA and used to assess the prognostics values of the CCP tests. RESULTS: At a similar specificity the CCP2 test had a higher sensitivity than the CCP1 test. Both tests identified a subgroup of patients with RA with an increased rate of joint damage progression. The anti-CCP2 test identified more patients with an increased rate of joint damage progression than the anti-CCP1 test, and in multiple regression analysis CCP2 was the better predictor of joint damage. CONCLUSIONS: The CCP2 test had better diagnostic and prognostic ability than the CCP1 test. (+info)The three main subtypes of FASD are:
1. Fetal Alcohol Syndrome (FAS): This is the most severe form of FASD and is characterized by a combination of physical, behavioral, and cognitive abnormalities. Individuals with FAS often have facial abnormalities, growth retardation, and central nervous system defects.
2. Partial Fetal Alcohol Syndrome (pFAS): This subtype is characterized by some, but not all, of the physical and behavioral characteristics of FAS.
3. Alcohol-Related Birth Defects (ARBD): This subtype includes individuals who have physical birth defects caused by prenatal alcohol exposure, but do not meet the full criteria for FAS or pFAS.
Other types of FASD include:
1. Neurobehavioral Disorder Associated with Prenatal Alcohol Exposure (ND-PAE): This subtype is characterized by behavioral and cognitive abnormalities, such as attention deficit hyperactivity disorder (ADHD), anxiety, and depression.
2. Maternal and Child Health Consensus Statement on FASD: This subtype includes individuals who have a history of prenatal alcohol exposure and exhibit a range of physical, behavioral, and cognitive abnormalities, but do not meet the full criteria for any of the other subtypes.
The diagnosis of FASD is based on a combination of clinical findings, medical history, and developmental assessments. There is no specific test or biomarker for FASD, so diagnosis can be challenging and requires expertise in pediatrics, neurology, and developmental psychopathology.
Treatment for FASD typically involves a multidisciplinary approach that includes medical care, behavioral interventions, and supportive services. Management of the condition may involve working with a team of healthcare professionals, such as pediatricians, neurologists, developmental specialists, and social workers.
The prognosis for individuals with FASD varies depending on the severity of their alcohol exposure during pregnancy, the timing and amount of exposure, and the presence of any comorbid conditions. However, early diagnosis and intervention can significantly improve outcomes and reduce the risk of long-term complications.
In summary, FASD is a complex and multifactorial condition that results from alcohol exposure during pregnancy. Diagnosis can be challenging, but a comprehensive evaluation and multidisciplinary approach to treatment can improve outcomes for individuals with FASD.
1. Alcohol Use Disorder (AUD): A diagnosis given to individuals who have difficulty controlling their alcohol consumption and experience negative consequences as a result.
2. Alcohol Dependence Syndrome (ADS): A condition characterized by a strong psychological and physiological dependence on alcohol, leading to withdrawal symptoms when alcohol use is stopped suddenly.
3. Alcohol-Induced Neurological Disorders: Conditions such as Wernicke-Korsakoff syndrome, which affects memory and coordination, and delirium tremens, a severe form of alcohol withdrawal that can be life-threatening.
4. Alcohol-Related Liver Disease (ALD): A condition characterized by fatty liver disease, alcoholic hepatitis, and cirrhosis, which can lead to liver failure and other complications.
5. Heart Disease: Excessive alcohol consumption can damage the heart muscle, increase blood pressure and triglycerides, and increase the risk of heart attack and stroke.
6. Mental Health Disorders: Alcohol can worsen symptoms of mental health conditions such as depression, anxiety, and post-traumatic stress disorder (PTSD).
7. Nutritional Deficiencies: Poor nutrition and malabsorption associated with heavy alcohol consumption can lead to deficiencies in essential vitamins and minerals.
8. Immune System Suppression: Chronic alcohol consumption can weaken the immune system, making individuals more susceptible to infections like pneumonia and tuberculosis.
9. Pancreatitis: A painful inflammatory condition of the pancreas that can be triggered by heavy alcohol consumption.
10. Various Cancers: Excessive alcohol consumption has been linked to an increased risk of several types of cancer, including liver, breast, colon, and throat cancer.
It is important to note that these risks are often dose-dependent, meaning that the more alcohol consumed, the greater the risk of developing these health problems. Additionally, binge drinking, or consuming large amounts of alcohol in a short period, can significantly increase the risk of acute injuries and death.
CAMP-dependent pathway
Cytidylate cyclase
Waterwheel Falls
Cyclic di-GMP-I riboswitch
Skin whitening
Adenosine
Activator (genetics)
Beta2-adrenergic agonist
Glycogenesis
Thromboregulation
CAMP responsive element modulator
CAMP receptor protein
8-Bromoguanosine 3',5'-cyclic monophosphate
3',5'-cyclic-AMP phosphodiesterase
Cyclic guanosine monophosphate
Piclamilast
Catabolite activator protein
Phosphodiesterase-4 inhibitor
Tropic cues involved in growth cone guidance
Chvostek sign
Deoxyadenosine monophosphate
Thompson submachine gun
Anthrax
Fungal behavior
HRASLS3
PDE4C
Adenosine monophosphate
Tullio Pozzan
Beta3-adrenergic agonist
Thermogenin
Bucladesine
Olfactory receptor neuron
Sandhya Srikant Visweswariah
Metabotropic glutamate receptor
Corn silk
Effects of cannabis
Sekai Holland
INPP5D
PDE4B
Olfactory receptor
Cystic fibrosis transmembrane conductance regulator
Acrasin
PDE4A
Transduction (physiology)
AKAP5
Metformin
David Fell (biochemist)
HCN4
Fructose 2,6-bisphosphate
Albright's hereditary osteodystrophy
Melatonin
Ribonucleotide
Benzene
Deficiency of RbAp48 protein and memory loss
H-89
Cyclic AMP receptors
RAPGEF2
General der Nachrichtenaufklärung
Syed Ziaur Rahman
Adenosine2A receptor vasodilation of rat preglomerular microvessels is mediated by EETs that activate the cAMP/PKA pathway
Platelet Disorders: Overview of Platelet Disorders, Pathophysiology of Platelet Disorders, Autoimmune Thrombocytopenias
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Publication Detail
Intracellular cyclic2
- Dopamine, by acting on the dopamine D 1 -like receptor, stimulates adenylyl cyclase activity to increase intracellular cyclic AMP (cAMP) levels [ 10 ], which stimulate cAMP-dependent protein kinase (PKA) [ 11 ]. (biomedcentral.com)
- Elevation of intracellular cyclic AMP levels leads to diverse cellular responses dependent on the cell type. (nottingham.ac.uk)
Adenosine triphosphate2
- This enzyme helps convert a molecule called adenosine triphosphate (ATP) to another molecule called cyclic adenosine monophosphate (cAMP). (medlineplus.gov)
- A receptor accepts a hormone and stimulates adenylyl cyclase (AC) to convert adenosine triphosphate (ATP) inside the cell to cyclic adenosine monophosphate (cAMP). (nih.gov)
Molecule5
- This enzyme is inhibited by high concentrations of caffeine, so it is possible that the stimulatory effect of this drug is the result of the raised cAMP levels that it causes (However it seems the concentrations required for caffeine to be effective are very high and a more likely explanation for the drug's effects involve the adenosine molecule). (dadamo.com)
- ATP is a molecule that supplies energy for cells' activities, including muscle contraction, and cAMP is involved in signaling for many cellular functions. (medlineplus.gov)
- These intracellular events are the result of a second messenger, another small molecule called cyclic AMP ( cAMP ) that stimulates enzyme production. (fsu.edu)
- Forskolin increases cellular levels of a molecule called cyclic adenosine monophosphate (cAMP). (supplementcentre.com)
- One theory is that brain cells with low levels of a molecule called cyclic AMP (cAMP) may cause depression. (nih.gov)
Nucleotide5
- This gene is a member of the type IV, cyclic AMP (cAMP)-specific, cyclic nucleotide phosphodiesterase (PDE) family. (nih.gov)
- 11. Relationships between chemotaxis, chemotactic modulators, and cyclic nucleotide levels in tumor cells. (nih.gov)
- 16. Proceedings: Effects of cyclic nucleotide monophosphates (cAMP, dbcAMP, cGMP, cIMP) on transepithelial netfluxes in proximal convolutions of rat kidneys. (nih.gov)
- A cyclic nucleotide formed from CYTIDINE TRIPHOSPHATE by the action of cytidylate cyclase. (nih.gov)
- It is a potential cyclic nucleotide intracellular mediator of signal transductions. (nih.gov)
Phosphodiesterase 4B1
- Using normal and malignant lymphocytes from humans, and the phosphodiesterase 4b (Pde4b) knockout mouse, we found that cAMP induces PD-L1 transcription and protein expression. (nih.gov)
Protein kinases1
- Cyclic AMP is involved in some protein kinases. (dadamo.com)
Cytidine1
- 18. Cytidine 3',5'-monophosphate (cyclic CMP). (nih.gov)
Monophosphate6
- CBP [cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB)-binding protein] is one of the most researched proteins for its therapeutic function. (nih.gov)
- 13. Adenosine 3': 5'-cyclic monophosphate as a possible mediator in the proliferative effect of prolactin on the pigeon crop sac. (nih.gov)
- Adhesion results in initial platelet activation by internal signalling pathways often involving reduced intra-platelet cyclic adenosine monophosphate. (nps.org.au)
- These findings have led to the suggestion that in these areas the DA-stimulated adenylate cyclase and the DA receptor may be related, and that the physiological effects of DA could be mediated by cyclic adenosine monophosphate (cAMP). (erowid.org)
- It is this second substance, cyclic adenosine monophosphate (cAMP), that stimulates the breakdown of stored carbohydrate into sugar. (nih.gov)
- The stimulation of cells with isoproterenol (7683592) in the presence of TDI failed to release cyclic-adenosine- monophosphate (cAMP). (cdc.gov)
Pathways3
- We do not yet know the discrete targets, in brain, of the NCS-Rapgef2/ERK-, PKA/CREB- and Epac/p38-specific cAMP signaling pathways elucidated in cellula . (nih.gov)
- These results implicate the myometrium as an essential regulator of endocrine hormone (cortisol and progesterone synthesis) and signaling pathways (cyclic AMP and cyclic GMP stimulation) that direct quiescence via the transcripitional upregulation of both novel and previously associated regulators. (biomedcentral.com)
- A number of these regulators stimulate cyclic AMP (cAMP)- and cGMP-mediated signaling pathways. (biomedcentral.com)
Synthesis1
- 20. Effects of cyclic nucleotides on hemoglobin synthesis in fetal calf liver cells in culture. (nih.gov)
Epithelial2
- 1. Cyclic nucleotides and the control of epithelial cell proliferation: cyclic CMP may be a partial mediator of the response of the pigeon crop-sac to prolactin. (nih.gov)
- Activation of G s -coupled receptors stimulate adenylyl cyclase leading to cyclic AMP (cAMP) production, which is known to induce mucus overproduction through the cAMP response element binding protein (CREB) in airway epithelial cells. (biomedcentral.com)
Exerts1
- Cyclic-AMP (cAMP) exerts suppressive effects in the innate and adaptive immune system. (nih.gov)
CREB2
- A recently constructed conditional PACAP knock-out mouse, in conjunction with Rapgef2- and CREB-conditional knockout mice, are being deployed to determine the cAMP effectors required in vivo for PACAP-dependent activation of the HPA axis, PACAP-dependent stress-induced hypophagia, and PACAP-dependent aversive responding. (nih.gov)
- Mechanistically, we discovered that the cAMP effectors PKA and CREB induce the transcription/secretion of IL-10, IL-8, and IL-6, which initiate an autocrine loop that activates the JAK/STAT pathway and ultimately increase PD-L1 expression in the cell surface. (nih.gov)
Endocrine1
- The lab has recently identified NCS-Rapgef2 as a novel cAMP effector linking Gs-coupled GPCR activation to activation of the MAP kinase ERK in neurons and endocrine cells. (nih.gov)
CGMP1
- 10. cAMP, cGMP, cCMP and cUMP concentrations across the tree of life: High cCMP and cUMP levels in astrocytes. (nih.gov)
Levels6
- When the genetically engineered mice were given a drug that increases cAMP levels (rolipram), they showed increased proteasome function, reduced aggregated tau levels, and improved cognitive performance. (nih.gov)
- Our long-term goal is to examine the parcellation of cAMP signaling during neurotransmission in the brain, at the genetic, cellular, morphological, and biochemical levels, and their penetrance to experience-driven behavior in the mouse. (nih.gov)
- We hypothesised that prostacyclin action could be enhanced by inhibition of phosphodiesterase type 3 (PDE3), a major regulator of cyclic AMP levels in the lung, whose activity appears increased in PAH [1]. (ucl.ac.uk)
- Elevated cAMP levels are associated with increased rates of fat loss and can improve the effects of other fat burning compounds. (supplementcentre.com)
- A drug called ketamine may increase the levels of cAMP in a person s brain cells. (nih.gov)
- To find out if administering ketamine to people with depression affects cAMP levels in their brains. (nih.gov)
Enzyme4
- cAMP decomposition into AMP is catalyzed by the enzyme Phosphodiesterase (PDE) . (dadamo.com)
- This occurs through inhibition of the cAMP-producing enzyme, adenylate cyclase, as a side effect of glucose transport into the cell. (dadamo.com)
- Some ADCY5 gene mutations that cause ADCY5 -related dyskinesia are thought to increase adenylate cyclase 5 enzyme activity and the level of cAMP within cells. (medlineplus.gov)
- An additional focus of my research has been an investigation of enzymes (particularly those involved in turnover of endocannabinoids, hydrogen sulphide and cyclic nucleotides), as convergence points for signalling cross-talk, as well as quantifying enzyme activities ex vivo , for example, in pathological conditions or following drug exposure. (nottingham.ac.uk)
Proteins1
- Cyclic AMP binds to specific locations on the regulatory units of the protein kinase, and causes dissociation between the regulatory and catalytic subunits, thus activating the catalytic units and enabling them to phosphorylate substrate proteins. (dadamo.com)
Elevation1
- In conclusion, PDE3 inhibition may help improve prostacyclin analogue action in IPAH by prolonging elevation in cAMP and enhancing the antiproliferative effects of these agents. (ucl.ac.uk)
Stimulation1
- To characterize the stimulation of cAMP through the dopamine D 1 receptor, 16HBE14o- cells and NCI-H292 cells were treated with dopamine or the dopamine D 1 receptor agonists (SKF38393 or A68930) before cAMP measurements. (biomedcentral.com)
Lymphocytes1
- 17. [Effect of cyclic nucleotides on the transformation and proliferation of lymphocytes]. (nih.gov)
Effectors1
- We have previously demonstrated that cAMP signaling is parcellated via multiple effectors in neuroendocrine cells. (nih.gov)
Adenylate cyclase1
- cAMP is synthesised from ATP by adenylate cyclase. (dadamo.com)
Proliferation2
- Transcription Factor Trps1 Promotes Tubular Cell Proliferation after Ischemia-Reperfusion Injury through cAMP-Specific 3',5'-Cyclic Phosphodiesterase 4D and AKT. (bvsalud.org)
- Cell proliferation (assessed by cell number) and cyclic AMP assays were performed in pulmonary arterial smooth muscle cells derived from patients with idiopathic PAH (n=6). (ucl.ac.uk)
Cells4
- 2. Effects of cyclic nucleotides on growth activity of V79-1A cells. (nih.gov)
- In fact, the activation of ERK by cyclic AMP, via NCS-Rapgef2, appears to be a unique feature of neurons and neuroendocrine cells in adult mammals. (nih.gov)
- MIN6-CB4 cells can serve as an invaluable tool for studying the regulatory mechanisms of insulin secretion, such as the GLP-1/cAMP signaling, in β-cells. (nature.com)
- Dopamine or the dopamine D 1 -like receptor agonists stimulated cAMP production in 16HBE14o- cells and NCI-H292 cells, which was reversed by the selective dopamine D 1 -like receptor antagonists (SCH23390 or SCH39166). (biomedcentral.com)
Increases1
- CRP-cAMP increases expression of a large number of genes, including some encoding enzymes that can supply energy independent of glucose. (dadamo.com)
Pathway1
- Proteasome function is activated by a pathway involving protein kinase A and cyclic AMP (cAMP). (nih.gov)
Mechanisms1
- Bell, D & McDermott, B 1994, ' Use of cyclic AMP antagonist Rp-cAMPS to distinguish between cyclic AMP-dependent and cyclic AMP independent contractile coupling mechanisms in mammalian ventricular cardiomyocytes ', Journal of Molecular and Cellular Cardiology , vol. 26, pp. 1439-1448. (qub.ac.uk)
Complex1
- The transcription factor CRP (or CAP) forms a complex with cAMP and thereby is activated to bind to DNA. (dadamo.com)
Effects1
- cAMP is a second messenger, used for intracellular signal transduction, such as transferring the effects of hormones like glucagon and adrenaline, which cannot get through the cell membrane. (dadamo.com)
Smooth1
- Smooth muscle contraction is inhibited by the phosphorylation of myosin light-chain kinase by the cAMP-dependent protein kinase. (biomedcentral.com)
Inhibition1
- In summary, we discovered that PD-L1 induction is a part of the repertoire of immunosuppressive actions mediated by cAMP, defined a cytokine-mediated autocrine loop that executes this action and, reassuringly, showed that PDE4 inhibition does not antagonize immune checkpoint blockade in an in vivo syngeneic lymphoma model. (nih.gov)
Dependent3
- For example, PKA (protein kinase A, also known as cAMP-dependent protein kinase) is normally inactive as a tetrameric holoenzyme, consisting of 2 catalytic and 2 regulatory units (C2R2), with the regulatory units blocking the catalytic centers of the catalytic units. (dadamo.com)
- PACAPergic synapses mediating stress-dependent relapse to cocaine preference in rodents are also being investigated, in the context of parcellated cAMP signaling in both the PACAP- and dopamine-dependent components of this translationally important behavior. (nih.gov)
- The cyclic AMP was assayed using the activation of a purified cAMP dependent protein kinase described by Kuo and Greengard (12). (erowid.org)
Action1
- 19. Central action of cyclic: 3',5'-thymidine, 3',5'-uridine and 3',5'-citidine monophosphates in rat. (nih.gov)
Growth1
- In bacteria, the level of cAMP varies depending on the medium used for growth. (dadamo.com)
Specific1
- Chromatin immunoprecipitation sequencing assays and RT-PCR revealed that Trps1 regulated cAMP-specific 3',5'-cyclic phosphodiesterase 4D (Pde4d) expression. (bvsalud.org)
Early2
Brain1
- Parcellated cyclic AMP signaling is likely to be functionally critical at neuropeptidergic, and catecholamine-modulated as well as glutamate-driven synapses in the brain. (nih.gov)