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This cGMP effect on DRG axon branching is specific, because 8-bromoadenosine-3′,5′-cyclic monophosphate (8-Br-cAMP), an equivalent analog to activate the cAMP pathway, did not elicit the same effect (Fig. 1G-I). Neither the distribution nor the average number of branching points changed significantly in the 8-Br-cAMP-treated culture compared with the untreated one (Fig. 1N,P). Furthermore, YC-1, a small molecule that activates the soluble guanylyl cyclase (sGC) to produce cGMP (Galle et al., 1999), induced branch formation in a dose dependent manner, reaching a similar level as in the 8-Br-cGMP-treated culture (Fig. 1J-L,O,P). Conversely, Zaprinast, an inhibitor that prevents cGMP degradation by phosphodiesterase-5 (Dundore et al., 1993), also induced branching (data not shown).. We further examined several parameters to determine if the in vitro effect reflects the role of cGMP signaling in axon growth or branching. First, neurons from the control cultures had a total length (Lt) of 254 ± ...

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Doherty, P J.; Tsao, J; Schimmer, B P.; Mumby, M C.; and Beavo, J A., Alteration of the regulatory subunit of type 1 camp-dependent protein kinase in mutant y1 adrenal cells resistant to 8-bromoadenosine 3:5-monophosphate. (1982). Subject Strain Bibliography 1982. 2372 ...

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Looking for online definition of cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) in the Medical Dictionary? cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) explanation free. What is cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP)? Meaning of cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) medical term. What does cyclic adenosine monophosphate (cyclic AMP, cAMP, 3',5'-cAMP) mean?

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Bovine leukemia virus (BLV) is a type C, chronic transforming retrovirus that infects B-lymphocytes and is associated with a long latency period. We studied the transcriptional activation of BLV in primary cells and also examined whether a measurable increase in BLV expression would effect the transcription of host genes. De novo protein synthesis was inhibited by cycloheximide (CHX) for 6 h after initiating peripheral blood leukocyte (PBL) cultures to eliminate Tax-mediated transcription. Under these conditions, transcription of the doubly spliced tax/rex message was predominant and was induced by the addition of phorbol 12-myristate 13-acetate (PMA), 8-bromo-cyclic AMP (Br-cAMP) and fetal bovine serum. Serum-induced BLV expression was inhibited in PBL in a dose dependent fashion by the protein kinase A (PKA) inhibitor H-89. Host gene expression was classified as labile protein-dependent when transcription was modulated by CHX and protein kinase-mediated when transcription was modulated by PMA, ...

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en] Murine AIDS (MAIDS) is caused by infection with the murine leukemia retrovirus RadLV-Rs and is characterized by T-cell anergy and severe immunodeficiency with increased susceptibilty to several experimental opportunistic infections as observed in HIV infection. T cell anergy is associated with an increase of intracellular cAMP level, triggering a multistep pathway involving activation of PKA type I and resulting in inhibition of proximal TCR signaling. We have reviously demonstrated that blocking PKA type I using the selective inhibitor Rp-8-Br-cAMPS, restores T-cell function in vitro in MAIDS as well as in HIV infection. In the present report, we investigated the effect of parenteral administration of Rp-8-Br-cAMPS in mice with MAIDS. We show that the compound is not toxic and partially restores the ex vivo proliferative responses to anti-CD3 mAb, but that it has no effect on the lymphadenopathy and splenomegaly characterizing ...

The primary reservoir for hepatitis C virus (HCV) replication is believed to be hepatocytes, which are highly polarized with tight junctions (TJ) separating their basolateral and apical domains. HepG2 cells develop polarity over time, resulting in the formation and remodeling of bile canalicular (BC) structures. HepG2 cells expressing CD81 provide a model system to study the effects of hepatic polarity on HCV infection. We found an inverse association between HepG2-CD81 polarization and HCV pseudoparticle entry. As HepG2 cells polarize, discrete pools of claudin-1 (CLDN1) at the TJ and basal/lateral membranes develop, consistent with the pattern of receptor staining observed in liver tissue. The TJ and nonjunctional pools of CLDN1 show an altered association with CD81 and localization in response to the PKA antagonist Rp-8-Br-cyclic AMPs (cAMPs). Rp-8-Br-cAMPs reduced CLDN1 expression at the basal membrane and inhibited HCV infection, supporting a model where the nonjunctional pools of CLDN1 ...

Cyclic adenosine monophosphate (cAMP) controls the physiological response to many diverse extracellular stimuli. To maintain signal specificity, cAMP-mediated signaling is finely tuned by means of a complex array of proteins that control the spatial and temporal dynamics of the second messenger within the cell. To unravel the way a cell encodes cAMP signals, new biosensors have recently been introduced that allow imaging of the second messenger in living cells with high spatial resolution. The more recent generation of such biosensors exploits the phenomenon of fluorescence resonance energy transfer between the green fluorescent protein- tagged subunits of a chimeric protein kinase A, as the way to visualize and measure the dynamic fluctuations of cAMP. This chapter describes the molecular basis on which such a genetically encoded cAMP sensor relies and the tools and methods required to perform cAMP measurements in living samples.

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R-CMP - R-Cytodine Monophosphate. Looking for abbreviations of R-CMP? It is R-Cytodine Monophosphate. R-Cytodine Monophosphate listed as R-CMP

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Adenosine Monophosphate: Adenylic acid. Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2-, 3-, or 5-position.

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The National Institute of Standards and Technology (NIST) uses its best efforts to deliver a high quality copy of the Database and to verify that the data contained therein have been selected on the basis of sound scientific judgment. However, NIST makes no warranties to that effect, and NIST shall not be liable for any damage that may result from errors or omissions in the Database ...

The National Institute of Standards and Technology (NIST) uses its best efforts to deliver a high quality copy of the Database and to verify that the data contained therein have been selected on the basis of sound scientific judgment. However, NIST makes no warranties to that effect, and NIST shall not be liable for any damage that may result from errors or omissions in the Database ...

There is considerable interest in the possible use of cAMP-elevating agents in the treatment of autoimmune diseases such as rheumatoid arthritis. The objective of this study was to evaluate the impact of different cAMP-elevating agents on the T-cell response to type II collagen within the context of collagen-induced arthritis, a murine model of rheumatoid arthritis. Spleen cells or lymph node cells from type-II-collagen-immunized DBA/1 mice were cultured in the presence of type II collagen plus one of five different cAMP-elevating agents: rolipram, forskolin, prostaglandin E2, 8-bromo-cAMP, or cholera toxin. Levels of interferon-gamma (IFN-gamma), interleukin-4 (IL-4) and IL-5 were measured in culture supernatants by enzyme-linked immunosorbent assay. All of the cAMP-elevating agents tested were found to profoundly suppress IFN-gamma production in a dose-dependent manner. IL-4 and IL-5 production was slightly up-regulated at low concentrations of the cAMP-elevating agents and was modestly suppressed at

In Schwann cells (SCs), cyclic adenosine monophosphate (cAMP) not only induces differentiation into a myelinating SC-related phenotype, but also synergistically enhances the mitogenic action of growth factors such as neuregulin. impairment of SC differentiation and myelin formation but not Krox-20 expression, which indicates an independent mechanism of Krox-20 regulation in response to cAMP. In conclusion, our data supports the idea that the outcome of cAMP signaling in SCs depends on the particular set of effectors activated. Whereas the mitogenic action of cAMP relies exclusively on PKA activity, the differentiating action of cAMP requires a PKA-independent (non-canonical) cAMP-specific pathway that is partially transduced by EPAC. Introduction The ubiquitous second messenger cyclic adenosine monophosphate (cAMP) is usually a key regulator of metabolic activity, survival, proliferation and differentiation in a wide variety of cell types. In particular, isolated cultured Schwann cells (SCs), ...

In humans, cAMP works by activating protein kinase A (PKA, cAMP-dependent protein kinase), one of the first few kinases discovered. It has four sub-units two catalytic and two regulatory. cAMP binds to the regulatory sub-units.[16] It causes them to break apart from the catalytic sub-units. The Catalytic sub-units make their way in to the nucleus to influence transcription.Further effects mainly depend on cAMP-dependent protein kinase, which vary based on the type of cell. cAMP-dependent pathway is necessary for many living organisms and life processes. Many different cell responses are mediated by cAMP; these include increase in heart rate, cortisol secretion, and breakdown of glycogen and fat. cAMP is essential for the maintenance of memory in the brain, relaxation in the heart, and water absorbed in the kidney.[17] This pathway can activate enzymes and regulate gene expression. The activation of preexisting enzymes is a much faster process, whereas regulation of gene expression is much longer ...

Protein Kinase A-Dependent Derepression of the Human Prodynorphin Gene via Differential Binding to an Intragenic Silencer Element: Induction of the prodynorphin

Toxicokinetic Assessment No specific study has been performed on the absorption/distribution/metabolism/excretion (ADME) of 2‑bromo‑3,3,3‑trifluoropropene (BTP).However, data are currently available from anin vitrovial equilibration method used to determine partition coefficients for blood and tissues andin vivotoxicology studies performed with this substance. 2‑bromo‑3,3,3‑trifluoropropene is a fire extinguisher agent, aclear liquid with a slight yellow tint,with a small molecular weight 174.95 and a Log P value of 2.7. It is very soluble (1000 mg/L).These physicochemical properties suggest that 2‑bromo‑3,3,3‑trifluoropropene will be readily absorbed across biological membranes via all routes. It is expected to have a high bioavailability but lack bioaccumulation properties.2‑Bromo‑3,3,3‑trifluoropropene is highly volatile and boils just below body temperature (recorded boiling point = 34.4°C) therefore it is expected that the inhalation route rather than the dermal ...

For other salt forms please inquire. Lipophilic site-selective cyclic AMP analogue with extremely high selectivity for site B of protein kinase A type II. Acts synergistically with site A activating analogues for selective activation of type II. Metabolic

Intracellular cAMP levels are higher in LDLR-/−p110γ−/− than in LDLR−/−p110γ+/−macrophages.LDLR−/−p110γ+/− and LDLR−/−p110γ−/− BMM

Adenosine monophosphate: | |Adenosine monophosphate| (|AMP|), also known as |5-adenylic acid|, is a |nucleotid... World Heritage Encyclopedia, the aggregation of the largest online encyclopedias available, and the most definitive collection ever assembled.

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Дофаминовый рецептор D1 - рецептор дофамина, сопряжённый с G-белками, стимулирующий аденилатциклазу и активирующий cAMP-зависимые киназы. В некоторых исследованиях отмечается ассоциация вариантов гена DRD1 с шизофренией, в других корреляции не обнаруживается[1]. Ген дофаминового рецептора D1 был впервые клонирован в 1990 году несколькими группами исследователей[2][3][4]. По результатам клонирования было установлено, что ген состоит из единственного экзона и кодирует белок из 446 аминокислотных остатков. Так же в первичной структуре соответствующего белка ...

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