2-Chloroadenosine: 2-Chloroadenosine. A metabolically stable analog of adenosine which acts as an adenosine receptor agonist. The compound has a potent effect on the peripheral and central nervous system.Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.Secosteroids: Steroids in which fission of one or more ring structures and concomitant addition of a hydrogen atom at each terminal group has occurred.Adenosine-5'-(N-ethylcarboxamide): A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.Xanthines: Purine bases found in body tissues and fluids and in some plants.Receptors, Purinergic P1: A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).Phenylisopropyladenosine: N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.Purinergic P1 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.Theophylline: A methyl xanthine derivative from tea with diuretic, smooth muscle relaxant, bronchial dilation, cardiac and central nervous system stimulant activities. Theophylline inhibits the 3',5'-CYCLIC NUCLEOTIDE PHOSPHODIESTERASE that degrades CYCLIC AMP thus potentiates the actions of agents that act through ADENYLYL CYCLASES and cyclic AMP.Purinergic P1 Receptor Agonists: Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.8-Bromo Cyclic Adenosine Monophosphate: A long-acting derivative of cyclic AMP. It is an activator of cyclic AMP-dependent protein kinase, but resistant to degradation by cyclic AMP phosphodiesterase.Phenethylamines: A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)Receptor, Adenosine A2B: A subclass of adenosine A2 receptors found in the CECUM, the COLON, the BLADDER, and a variety of other tissues. It is generally considered to be a low affinity receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.Pyran Copolymer: Copolymer of divinyl ether and maleic anhydride that acts as an immunostimulant with antineoplastic and anti-infective properties. It is used in combination with other antineoplastic agents.Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752)Purinergic Antagonists: Drugs that bind to and block the activation of PURINERGIC RECEPTORS.Tubercidin: An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.Adenosine Kinase: An enzyme that catalyzes the formation of ADP plus AMP from adenosine plus ATP. It can serve as a salvage mechanism for returning adenosine to nucleic acids. EC 2.7.1.20.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Receptor, Adenosine A2A: A subclass of adenosine A2 receptors found in LEUKOCYTES, the SPLEEN, the THYMUS and a variety of other tissues. It is generally considered to be a receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.Muscarine: A toxic alkaloid found in Amanita muscaria (fly fungus) and other fungi of the Inocybe species. It is the first parasympathomimetic substance ever studied and causes profound parasympathetic activation that may end in convulsions and death. The specific antidote is atropine.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
(1/208) Interruption of transmembrane signaling as a novel antisecretory strategy to treat enterotoxigenic diarrhea.

Bacteria that produce heat-stable enterotoxins (STs), a leading cause of secretory diarrhea, are a major cause of morbidity and mortality worldwide. ST stimulates guanylyl cyclase C (GCC) and accumulation of intracellular cyclic GMP ([cGMP]i), which opens the cystic fibrosis transmembrane conductance regulator (CFTR)-related chloride channel, triggering intestinal secretion. Although the signaling cascade mediating ST-induced diarrhea is well characterized, antisecretory therapy targeting this pathway has not been developed. 2-ChloroATP (2ClATP) and its cell-permeant precursor, 2-chloroadenosine (2ClAdo), disrupt ST-dependent signaling in intestinal cells. However, whether the ability to disrupt guanylyl cyclase signaling translates into effective antisecretory therapy remains untested. In this study, the efficacy of 2ClAdo to prevent ST-induced water secretion by human intestinal cells was examined. In Caco-2 human intestinal cells, ST increased [cGMP]i, induced a chloride current, and stimulated net basolateral-to-apical water secretion. This effect on chloride current and water secretion was mimicked by the cell-permeant analog of cGMP, 8-bromo-cGMP. Treatment of Caco-2 cells with 2ClAdo prevented ST-induced increases in [cGMP]i, chloride current and water secretion. Inhibition of the downstream consequences of ST-GCC interaction reflects proximal disruption of cGMP production because 8-bromo-cGMP stimulated chloride current and water secretion in 2ClAdo-treated cells. Thus, this study demonstrates that disruption of guanylyl cyclase signaling is an effective strategy for antisecretory therapy and provides the basis for developing mechanism-based treatments for enterotoxigenic diarrhea.  (+info)

(2/208) Depletion of alveolar macrophages by treatment with 2-chloroadenosine aerosol.

Alveolar macrophages (AMs) are localized in the alveoli and alveolar ducts of the lung and are the only macrophages living in an aerobic environment. Recent studies have demonstrated that AMs play a central role in lung diseases, such as pneumonia and acute respiratory distress syndrome. It has become important to find a simple, effective way to eliminate AMs in order to investigate the function of AMs in vivo. 2-Chloroadenosine (2-CA), a purine analog, is reported to be selectively cytotoxic to cultured macrophages, and we hypothesized that it would deplete the number of AMs in the bronchoalveolar lavage fluid (BALF) of mice without any effect on neutrophil or lymphocyte counts. After mice had inhaled 1 mM aerosolized 2-CA for 2 h, AMs were found to be significantly depleted at 0 h [(4.42 +/- 0.16) x 10(4)/ml], 24 h [(4.17 +/- 0.89) x 10(4)/ml], 48 h [(3.17 +/- 0.21) x 10(4)/ml], and 72 h [(5.00 +/- 0.64) x 10(4)/ml] compared with concentrations in untreated controls [(12.1 +/- 0.21) x 10(4)/ml]. Neutrophil and lymphocyte counts in BALF did not change and histological changes in the lung were not observed after 2-CA treatment. The lung wet-to-dry weight ratio did not change at 0, 24, and 48 h after 2-CA aerosol application. The 2-CA aerosol had no effect on lung vascular permeability, as assessed by the intravenous administration of Evans blue, or on other phagocytes, as assessed by Kupffer cell counts. Our study demonstrates the efficacy of 2-CA in reducing AM numbers in vivo.  (+info)

(3/208) A(2B) receptors mediate antimitogenesis in vascular smooth muscle cells.

Adenosine inhibits growth of vascular smooth muscle cells. The goals of this study were to determine which adenosine receptor subtype mediates the antimitogenic effects of adenosine and to investigate the signal transduction mechanisms involved. In rat aortic vascular smooth muscle cells, platelet-derived growth factor-BB (PDGF-BB) (25 ng/mL) stimulated DNA synthesis ([(3)H]thymidine incorporation), cellular proliferation (cell number), collagen synthesis ([(3)H]proline incorporation), total protein synthesis ([(3)H]leucine incorporation), and mitogen-activated protein (MAP) kinase activity. The adenosine receptor agonists 2-chloroadenosine and 5'-N-methylcarboxamidoadenosine, but not N(6)-cyclopentyladenosine or CGS21680, inhibited the growth effects of PDGF-BB, an agonist profile consistent with an A(2B) receptor-mediated effect. The adenosine receptor antagonists KF17837 and 1,3-dipropyl-8-p-sulfophenylxanthine, but not 8-cyclopentyl-1, 3-dipropylxanthine, blocked the growth-inhibitory effects of 2-chloroadenosine and 5'-N-methylcarboxamidoadenosine, an antagonist profile consistent with an A(2) receptor-mediated effect. Antisense, but not sense or scrambled, oligonucleotides to the A(2B) receptor stimulated basal and PDGF-induced DNA synthesis, cell proliferation, and MAP kinase activity. Moreover, the growth-inhibitory effects of 2-chloroadenosine, 5'-N-methylcarboxamidoadenosine, and erythro-9-(2-hydroxy-3-nonyl) adenine plus iodotubericidin (inhibitors of adenosine deaminase and adenosine kinase, respectively) were abolished by antisense, but not scrambled or sense, oligonucleotides to the A(2B) receptor. Our findings strongly support the hypothesis that adenosine causes inhibition of vascular smooth muscle cell growth by activating A(2B) receptors coupled to inhibition of MAP kinase activity. Pharmacological or molecular biological activation of A(2B) receptors may prevent vascular remodeling associated with hypertension, atherosclerosis, and restenosis following balloon angioplasty.  (+info)

(4/208) Altered regulation of potassium and calcium channels by GABA(B) and adenosine receptors in hippocampal neurons from mice lacking Galpha(o).

To examine the role of G(o) in modulation of ion channels by neurotransmitter receptors, we characterized modulation of ionic currents in hippocampal CA3 neurons from mice lacking both isoforms of Galpha(o). In CA3 neurons from Galpha(o)(-/-) mice, 2-chloro-adenosine and the GABA(B)-receptor agonist baclofen activated inwardly rectifying K(+) currents and inhibited voltage-dependent Ca(2+) currents just as effectively as in Galpha(o)(+/+) littermates. However, the kinetics of transmitter action were dramatically altered in Galpha(o)(-/-) mice in that recovery on washout of agonist was much slower. For example, recovery from 2-chloro-adenosine inhibition of calcium current was more than fourfold slower in neurons from Galpha(o)(-/-) mice [time constant of 12.0 +/- 0.8 (SE) s] than in neurons from Galpha(o)(+/+) mice (time constant of 2.6 +/- 0.2 s). Recovery from baclofen effects was affected similarly. In neurons from control mice, effects of both baclofen and 2-chloro-adenosine on Ca(2+) currents and K(+) currents were abolished by brief exposure to external N-ethyl-maleimide (NEM). In neurons lacking Galpha(o), some inhibition of Ca(2+) currents by baclofen remained after NEM treatment, whereas baclofen activation of K(+) currents and both effects of 2-chloro-adenosine were abolished. These results show that modulation of Ca(2+) and K(+) currents by G protein-coupled receptors in hippocampal neurons does not have an absolute requirement for Galpha(o). However, modulation is changed in the absence of Galpha(o) in having much slower recovery kinetics. A likely possibility is that the very abundant Galpha(o) is normally used but, when absent, can readily be replaced by G proteins with different properties.  (+info)

(5/208) Possible role of immune surveillance at the initial phase of metastasis produced by B16BL6 melanoma cells.

The relationship among the real-time trafficking of lung metastatic B16BL6 cells, metastatic potential, and the injected number of the cells was examined, since the smaller the number of tumor cells injected, the more clearly the immune defense may be observed. When 1x10(6) or 1x10(5) B16BL6 cells were injected into mice via the tail vein, both numbers of cells accumulated in the lung at a similar rate: there was an approximately 10-fold difference in the number of accumulated cells between the two doses. Elimination from the lung was not dependent on the cell number but on the proportion of accumulated cells. However, the injection of 1x10(4) cells resulted in lung accumulation less than one-tenth of that obtained with 1x10(5) cell injection. Metastasis was observed when 1x10(5) or 1x10(6) B16BL6 cells were injected, but not after injection of 1x10(4) cells. To clarify the roles of the immune defense system at the initial phase of metastasis, we challenged macrophage-depleted mice with 1x10(4) tumor cells. Treatment of mice with 2-chloroadenosine prior to the tumor cell challenge cancelled the suppression of not only metastasis but also the lung accumulation. Furthermore, the administration of 2-chloroadenosine following the tumor cell challenge had little effect on the metastatic potential. These results suggest that the immune surveillance whose action was obvious at the low dose of challenged tumor cells functions strongly at the initial phase but not at the advanced stages of the metastatic process, and that macrophages play an important role in the suppression of metastasis.  (+info)

(6/208) Adenosine A(2A) and A(2B) receptors in cultured human and porcine coronary artery endothelial cells.

We investigated the role of the cAMP link to the signal transduction mechanism coupled with adenosine A(2A) and A(2B) receptors in cultured human coronary artery endothelial cells (HCAEC) and porcine coronary artery endothelial cells (PCAEC). 2-[4-[2- inverted question mark2-[(4-aminophenyl)methylcarbonylamino]ethylaminocarbon yl inverted question marketh yl]phenyl]ethylamino-5'- ethylcarboxamidoadenosine ((125)I-PAPA-APEC) (PAPA-APEC) was used to demonstrate the specific binding in PCAEC membranes. The specific binding was saturable and reversible with a maximal number of binding sites (B(max)) of 240 fmol/mg protein, and scatchard analysis revealed a single class of binding site with an equilibrium dissociation constant (K(d)) of 1. 17 +/- 0.035 nM. In competition experiments, adenosine receptor agonists showed the following order of potency (based on IC(50)): 5'-(N-ethylcarboxamido)adenosine (NECA) >/= CGS-21680 > 2-chloroadenosine. This order appears to be consistent with the A(2) adenosine receptor classification. We also studied the effects of adenosine agonists on the accumulation of cAMP as an indirect approach to show the presence of functional A(2) receptors. Similarly, the same adenosine agonists (10(-7)-10(-4) M) elicited the production of cAMP in intact endothelial cells in a dose-dependent manner, exhibiting consistently with the A(2) adenosine receptor classification. A selective A(2A) adenosine receptor antagonist (ZM-241385, 10(-8) M) significantly inhibited the effect of CGS-21680 on cAMP but only partly inhibited the effect of NECA, suggesting the presence of both A(2A) and A(2B) receptors. Western blot analysis further showed the immunoreactivity of A(2A) and A(2B) receptor at 45 and 36 kDa, respectively, in both HCAEC and PCAEC. Direct evidence for the presence of A(2A) and A(2B) receptors in cultured HCAEC and PCAEC by reverse transcription-polymerase chain reaction (RT-PCR), revealed expected PCR product sizes (205 and 173 bp) for A(2A) and A(2B) receptors in HCAEC and PCAEC, respectively. The data show that adenylate cyclase-coupled adenosine A(2A) and A(2B) receptors are present in coronary endothelial cells.  (+info)

(7/208) Selective transport of adenosine into porcine coronary smooth muscle.

Adenosine (ADO), an endogenous regulator of coronary vascular tone, enhances vasorelaxation in the presence of nucleoside transport inhibitors such as dipyridamole. We tested the hypothesis that coronary smooth muscle (CSM) contains a high-affinity transporter for ADO. ADO-mediated relaxation of isolated large and small porcine coronary artery rings was enhanced 12-fold and 3.4-fold, respectively, by the transport inhibitor, S-(4-nitrobenzyl)-6-thioinosine (NBTI). Enhanced relaxation was independent of endothelium and was selective for ADO over synthetic analogs. Uptake of [(3)H]ADO into freshly dissociated CSM cells or endothelium-denuded rings was linear and concentration dependent. Kinetic analysis yielded a maximum uptake (V(max)) of 67 +/- 7.0 pmol. mg protein(-1). min(-1) and a Michaelis constant (K(m)) of 10. 5 +/- 5.8 microM in isolated cells and a V(max) of 5.1 +/- 0.5 pmol. min(-1). mg wet wt(-1) and a K(m) of 17.6 +/- 2.6 microM in intact rings. NBTI inhibited transport into small arteries (IC(50) = 42 nM) and cells. Analyses of extracellular space and diffusion kinetics using [(3)H]sucrose indicate the V(max) and K(m) for ADO transport are sufficient to clear a significant amount of extracellular adenosine. These data indicate CSM possess a high-affinity nucleoside transporter and that the activity of this transporter is sufficient to modulate ADO sensitivity of large and small coronary arteries.  (+info)

(8/208) A1 adenosine receptors inhibit multiple voltage-gated Ca2+ channel subtypes in acutely isolated rat basolateral amygdala neurons.

1. The anticonvulsant properties of 2-chloroadenosine (CADO) in the basolateral amygdala rely on the activation of adenosine-specific heptahelical receptors. We have utilized whole-cell voltage-clamp electrophysiology to examine the modulatory effects of CADO and other adenosine receptor agonists on voltage-gated calcium channels in dissociated basolateral amygdala neurons. 2. CADO, adenosine, and the A1 subtype-selective agonists N6-(L-2-Phenylisopropyl)adenosine (R-PIA) and 2-chloro-N6-cyclopentyladenosine (CCPA) reversibly modulated whole cell Ba2+ currents in a concentration-dependent fashion. CADO inhibition of barium currents was also sensitive to the A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). 3. The A2A-selective agonist 4-[2-[[6-Amino-9-(N-ethyl-beta-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl ]benzenepropanoic acid (CGS21680) was without effect. 4. CADO inhibition was predominantly voltage-dependent and sensitive to the sulphydryl-modifying reagent N:-ethylmaleimide, implicating a membrane-delimited, G(i/o)-coupled signal transduction pathway in the channel regulation. 5. Using Ca2+ channel subtype-selective antagonists, CADO inhibition appeared to target multiple channel subtypes, with the inhibition of omega-conotoxin GVIA-sensitive calcium channels being more prominent. 6. Our results indicate that the anti-convulsant effects CADO in the basolateral amygdala may be mediated, in part, by the A1 receptor-dependent inhibition of voltage gated calcium channels.  (+info)

*  Streptomyces rishiriensis
Charousová, Ivana; Javoreková, Soňa; Wink, Joachim (2 February 2015). "Isolation and characterization of Streptomyces ... Streptomyces rishiriensis produces coumermycin A1, notomycin, 2-chloroadenosine, phosphophenylalanarginine and lactonamycin. ...
*  List of MeSH codes (D13)
2-chloroadenosine MeSH D13.570.583.138.300.200 --- cladribine MeSH D13.570.583.138.325 --- deoxyadenosines MeSH D13.570.583.138 ... 2-chloroadenosine MeSH D13.570.800.096.300.200 --- cladribine MeSH D13.570.800.096.500 --- isopentenyladenosine MeSH D13.570. ...
The nucleoside analogues 8-amino-adenosine and 8-chloro-adenosine have been investigated in the | Beneficial Effects of RAF...  The nucleoside analogues 8-amino-adenosine and 8-chloro-adenosine have been investigated in the | Beneficial Effects of RAF...
The nucleoside analogues 8-amino-adenosine and 8-chloro-adenosine have been investigated in the. The nucleoside analogues 8- ... Intro The book nucleoside analogues 8-amino-adenosine (8-NH2-Ado) and 8-chloro-adenosine (8-Cl-Ado) possess undergone extensive ... The nucleoside analogues 8-amino-adenosine and 8-chloro-adenosine have been investigated in the ... and 8-chloro-adenosine but inadequate to induce level of resistance in delicate cells. Taken collectively, these results reveal ...
more infohttp://biodiversityhotspot.org/2017/08/the-nucleoside-analogues-8-amino-adenosine-and-8-chloro-adenosine-have-been-investigated-in-the/
2-Chloroadenosine (CADO) | Abcam  2-Chloroadenosine (CADO) | Abcam
Buy 2-Chloroadenosine (CADO) (CAS 146-77-0), an adenosine receptor agonist. Join researchers using high quality 2- ... Effect of intraperitoneal and intrahippocampal (CA1) 2-chloroadenosine in amygdaloid kindled rats.. Brain Res 751:259-64 (1997 ...
more infohttp://www.abcam.com/2-chloroadenosine-cado-ab120037.html
2-chloroadenosine-5-triphosphate | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY  2-chloroadenosine-5-triphosphate | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY
2-chloroadenosine-5-triphosphate ligand page. Quantitative data and detailed annnotation of the targets of licensed and ...
more infohttp://www.guidetopharmacology.org/GRAC/LigandDisplayForward?tab=refs&ligandId=1716
2-chloroadenosine-5-triphosphate | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY  2-chloroadenosine-5-triphosphate | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY
2-chloroadenosine-5-triphosphate ligand page. Quantitative data and detailed annnotation of the targets of licensed and ... 2R,3S,4R,5R)-5-(6-amino-2-chloropurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methyl (hydroxy-phosphonooxyphosphoryl) hydrogen phosphate ...
more infohttp://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1716
Signal Transduction Reagents - Agonists - Alfa Aesar  Signal Transduction Reagents - Agonists - Alfa Aesar
|p|Agonists are substances that activate cellular receptor molecules to which they attach. In a nutshell, agonists bind to cellular receptors and elicit a biological response. The agonists enhance the signal transduction by binding to the receptor in cellular systems. They can be full agonists, activating the receptor to maximal activity, or partial agonists. There are also inverse agonists. These ligands bind receptors and cause the reverse biological response of the natural ligand. Alfa Aesar supplies receptor agonists for many different cellular protein receptors. These reagents include both natural receptor ligands as well as synthetic agonists. In addition, the conformational changes brought about by the agonists activate or increase the activation of secondary intracellular messenger.|/p|
more infohttps://www.alfa.com/en/signal-transduction-reagents-agonists/
Adenosine, 2-chloro  Adenosine, 2-chloro
InChI=1S/C10H12ClN5O4/c11-10-14-7(12)4-8(15-10)16(2-13-4)9-6(19)5(18)3(1-17)20-9/h2-3,5-6,9,17-19H,1H2,(H2,12,14,15) ... Other names: Cl AS; 2 ClAdo; 2-Chloroadenosine; Cl-Ado; 2-chloroadenosinehemihydrate ... Adenosine, 2-chloro-. *Formula: C10H12ClN5O4 ...
more infohttps://webbook.nist.gov/cgi/cbook.cgi?ID=146-77-0&Units=SI&cMS=on
Neuromodulator-mediated phosphorylation of specific proteins in a neurotumor hybrid cell line (NCB-20). | CureHunter  Neuromodulator-mediated phosphorylation of specific proteins in a neurotumor hybrid cell line (NCB-20). | CureHunter
D-Ala2,D-Leu5]-enkephalin, which decreased cyclic AMP levels and reversed the 2-chloroadenosine-stimulated phosphorylation of ... NCB-20 cells were labeled with [32P]orthophosphate under conditions where 2-chloroadenosine gave maximum increases of 32P ...
more infohttp://www.curehunter.com/public/pubmed2450174.do
Design, Synthesis, and Evaluation of Genistein Analogues as Anti-Cancer Agents | BenthamScience  Design, Synthesis, and Evaluation of Genistein Analogues as Anti-Cancer Agents | BenthamScience
2-Chloroadenosine and Human Prostate Cancer Cells. Anti-Cancer Agents in Medicinal Chemistry ...
more infohttp://www.eurekaselect.com/131510
The Potential of Flavonolignans in Prostate Cancer Management | Bentham Science  The Potential of Flavonolignans in Prostate Cancer Management | Bentham Science
2-Chloroadenosine and Human Prostate Cancer Cells. Anti-Cancer Agents in Medicinal Chemistry ...
more infohttp://www.eurekaselect.com/145018/article?tracking-code=4
Adenosine A3 Receptor Deficiency Exerts Unanticipated Protective Effects on the Pressure-Overloaded Left Ventricle | Circulation  Adenosine A3 Receptor Deficiency Exerts Unanticipated Protective Effects on the Pressure-Overloaded Left Ventricle | Circulation
Adenosine exerts multiple functions through activation of individual adenosine receptor subtypes.2-5 A1 receptors (A1R) and A3 ... Our finding that A3R KO attenuated the TAC-induced increase of COX-2 and tended to decrease TNF-α after TAC supports a role for ... Male C57BL/6 (Taconic, Germantown, NY) body weight-matched A3R KO mice2 (crossed back to Taconic C57BL/6 mice at least 16 times ... However, the A3R agonist 2-chloro-N6-(3-iodobenzyl)adenosine-5′-N-methylcarboxamide (Cl-IB-MECA) or adenosine dose- and time- ...
more infohttp://circ.ahajournals.org/content/118/17/1713
Adenosine | Hello Bio  Adenosine | Hello Bio
Buy low cost, high quality adenosine receptor tools from Hello Bio. A trusted, affordable life science reagent supplier. Up to 50% less than other suppliers.
more infohttps://www.hellobio.com/products/target/receptors-transporters/g-protein-coupled-receptors/adenosine.html
Streptomyces rishiriensis - Wikipedia  Streptomyces rishiriensis - Wikipedia
Charousová, Ivana; Javoreková, Soňa; Wink, Joachim (2 February 2015). "Isolation and characterization of Streptomyces ... Streptomyces rishiriensis produces coumermycin A1, notomycin, 2-chloroadenosine, phosphophenylalanarginine and lactonamycin. ...
more infohttps://en.wikipedia.org/wiki/Streptomyces_rishiriensis
British Library EThOS: A neuropharmcological study of some aspects of carotid body chemoreceptor activity in the cat  British Library EThOS: A neuropharmcological study of some aspects of carotid body chemoreceptor activity in the cat
It was found that intracarotid injections of adenosine: AMP; ADP; ATP; CoA;Me-adenosine analogues: N6-methyladenosine, 2- ... chloroadenosine, 3'-deoxyudenosine but not 2'-deoxyadenosine; cyclic AMP; dibutyryl cyclic AMP increased spontaneous ...
more infohttp://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.661090
Table of Contents - April 01, 1997, 281 (1) | Journal of Pharmacology and Experimental Therapeutics  Table of Contents - April 01, 1997, 281 (1) | Journal of Pharmacology and Experimental Therapeutics
Putative kappa-2 Opioid Agonists Are Antihyperalgesic in a Rat Model of Inflammation Janice Ho, Andrew J. Mannes, Ronald Dubner ... Somatostatin Inhibition of Acid and Histamine Release by Activation of Somatostatin Receptor Subtype 2 Receptors in Rats K. ... Identification of Insulin-Like Growth Factor Binding Protein-2 as a Biochemical Surrogate Marker for the in Vivo Effects of ... In Vivo Evidence for Carrier-Mediated Efflux Transport of 3′-Azido-3′-Deoxythymidine and 2′,3′-Dideoxyinosine Across the Blood- ...
more infohttp://jpet.aspetjournals.org/content/281/1
Transferable anticancer innate immunity in spontaneous regression/complete resistance mice | PNAS  Transferable anticancer innate immunity in spontaneous regression/complete resistance mice | PNAS
2A). Fig. 2 B and C shows examples of PMN, MΦ, and NK surrounding S180 in rosettes. In contrast, CD8+ and CD4+ T cells and ... Tumor volume (V) was calculated by using the formula V = (W× W× L)/2, where W was the shorter of the two diameters and L was ... 2. Formation of leukocyte rosettes during the killing of cancer cells in SR/CR mice. SR/CR mice were challenged i.p. with 107 ... For PMN depletion, three i.p. injections of 500 μg of anti-Ly6G (10) were given to each SR/CR mouse at 2-day intervals. For NK ...
more infohttp://www.pnas.org/content/103/20/7753.full
Microcirculation and Mitochondrial Function in Focal Brain Ischemia | SpringerLink  Microcirculation and Mitochondrial Function in Focal Brain Ischemia | SpringerLink
Dora, E., 1985c, Effect of adenosine and its stabile analogue 2-chloroadenosine on cerebrocortical microcirculation and NAD/ ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4684-5188-7_26
Plus it  Plus it
The adenosine analogs, 5'-N-ethylcarboxamidoadenosine (NECA) and 2-chloroadenosine (CAD) caused concentration-dependent ...
more infohttp://jpet.aspetjournals.org/content/251/3/943
MEDICA  MEDICA
Adenosine;Guinea Pigs;Adenylyl Cyclases;Colforsin;Histamine;Cyclic AMP;2-Chloroadenosine;Norepinephrine; Synaptosomes;Receptors ... beta-2;Up-Regulation;Receptors, Adrenergic, alpha;Signal Transduction ...
more infohttp://digital.library.musc.edu/cdm/search/searchterm/forskolin/mode/all/order/subjec
Plus it  Plus it
Transporter function was assessed by the site-specific binding of [3H]NBMPR and the cellular uptake of [3H]2-chloroadenosine. ...
more infohttp://molpharm.aspetjournals.org/content/early/2012/07/26/mol.112.079616
  • 2-5 A 1 receptors (A 1 R) and A 3 receptors (A 3 R) are expressed in cardiomyocytes, and a substantial body of evidence indicates that adenosine can protect the heart during and after an ischemic insult. (ahajournals.org)
  • Klapstein, G.J. and Colmers, W.F. (1992) 4-Aminopyridine and low Ca++ differentiate presynaptic inhibition mediated by Neuropeptide Y, Baclofen and 2-Chloroadenosine in rat hippocampal CA1 in vitro. (tu.edu)
  • The brain was removed and placed in ice-cold solution (120 m m NaCl, 3.5 m m KCl, 0.7 m m CaCl 2 , 4 m m MgCl 2 , 1.25 m m NaH 2 PO 4 , 26 m m NaHCO 3 , and 10 m m glucose) bubbled with 95% O 2 /5% CO 2 . (jneurosci.org)
  • EXP BRAIN RES , 49 (2) 174 - 180. (ucl.ac.uk)
  • Male C57BL/6 (Taconic, Germantown, NY) body weight-matched A 3 R KO mice 2 (crossed back to Taconic C57BL/6 mice at least 16 times), 8 to 12 weeks old, were used for TAC or control. (ahajournals.org)
  • Spontaneous regression/complete resistance (SR/CR) mice possess a unique autosomal dominant trait that allows them to survive challenges with aggressive mouse cancer cells at up to millions of times the lethal doses for WT mice ( 1 , 2 ). (pnas.org)
  • Klapstein, G.J. and Levine, M.S. (2005) Age-dependent biphasic changes in ischemic sensitivity in the striatum of Huntington's Disease R6/2 transgenic mice. (tu.edu)
  • In 0.5-min incubations 2-chloroadenosine was less effective than adenosine at concentrations below 20 µM and more effective at concentrations above 100 µM. (aspetjournals.org)
  • 5. The method of claim 2, wherein said effective concentration is achieved by intravenous administration to a mammal. (google.es)
  • The respective ED₅₀ values for 2-ClAdo and theophylline were similar regardless of the chemoconvulsant used. (oregonstate.edu)