Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A nonequilibrium isoelectric focusing method incorporating the chemical spacers MOPS and HEPES was developed and subsequently evaluated for its ability to reliably discriminate common and rare phenotypes in the esterase D (EsD), red cell acid phosphatase (AcP1), phosphoglucomutase (PGM1), adenylate kinase (AK), and adenosine deaminase (ADA) isoenzyme systems. The validation procedures used were blind testing, comparison of results to conventional methods, and evaluation of known rare variant phenotypes. This method proved to be a quick and reliable method for typing all five isoenzyme systems, while providing an excellent probability of discrimination (PD = 0.96).
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PMID:Evaluation of a nonequilibrium isoelectric focusing (IEF) method for the simultaneous typing of esterase D (EsD), red cell acid phosphatase (AcP1), phosphoglucomutase (PGM1), adenylate kinase (AK), and adenosine deaminase (ADA). 215 93

There are four types of horizontal cell in the goldfish retina, three cone- and one rod-type. The neurotransmitter of only one type, the H1 (cone) horizontal cell, has been identified as GABA. 3H-adenosine uptake was examined as a possible marker for the other classes of horizontal cell. Isolated goldfish retinae were incubated in 3H-adenosine (10-40 microCi) in HEPES-buffered saline for 30 min, then fixed, embedded in plastic, and processed for light-microscopic autoradiography (ARG). For double-label immuno/ARG studies, 1-micron-thick sections were processed for GABA postembed immunocytochemistry, then for ARG. 3H-adenosine uptake was localized to cone photoreceptors, presumed precursor cells in the proximal outer nuclear layer, and to a single, continuous row of horizontal cell bodies in the inner nuclear layer. No uptake was localized to the region of horizontal cell axon terminals. 3H-adenosine uptake did not colocalize with GABA-IR in H1 horizontal cells, but it did colocalize with adenosine deaminase immunoreactivity. It is concluded that 3H-adenosine uptake selectively labels rod horizontal cells in the goldfish retina based on position and staining pattern, which are similar to rod horizontal cells stained by Golgi or HRP injection methods. The use of 3H-adenosine uptake may provide a useful tool to study other properties of rod horizontal cells (i.e. development) as well as provide clues as to the transmitter used by these interneurons.
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PMID:3H-adenosine uptake selectively labels rod horizontal cells in goldfish retina. 914 73

A detailed understanding of adenosine metabolism of vascular smooth muscle cells (VSMC) is highly desirable to critically evaluate possible autocrine effects of adenosine in this cell species. Therefore, this study quantified intra- and extracellular adenosine flux rates, the transmembrane concentration gradient, and the adenosine surface concentration in porcine VSMC and, for comparison, aortic endothelial cells (PAEC). Cell-covered microcarrier beads packed in a chromatography column were superfused with a HEPES buffer. With the use of specific inhibitors of adenosine kinase (iodotubericidine, 10 microM), adenosine deaminase [erythro-9-(2-hydroxy-3-nonyl)-adenine, 5 microM], ecto-5'-nucleotidase (alpha,beta-methylene-adenosine 5'-diphosphate, 50 microM), and adenosine membrane transport (n-nitrobenzylthioinosine, 1 microM), total production rates of 12.3 +/- 2.7 and 7.5 +/- 1.3 pmol x min(-1) x microl cell volume(-1) were obtained for VSMC and PAEC, respectively. Despite prevailing intracellular adenosine production (76 and 70% of total production, respectively), transmembrane concentration gradients under control conditions were directed toward the cytosol as a result of rapid intracellular adenosine rephosphorylation and continuous extracellular hydrolysis from 5'-AMP. Surface concentrations were approximately 18 nM in VSMC and PAEC under control conditions and increased to approximately 60 nM during partial inhibition of adenosine metabolism. Simultaneously, the transmembrane adenosine concentration gradient was reversed. We conclude that adenosine flux rates in VSMC and PAEC are quantitatively similar and that VSMC may influence the interstitial adenosine concentration under basal steady-state conditions.
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PMID:Significance of adenosine metabolism of coronary smooth muscle cells. 1112 25

The present study determined whether porcine leptin can alter the lipolytic rate in porcine adipocytes produced in vitro. The stromal-vascular cell fraction of neonatal subcutaneous adipose tissue was isolated by collagenase digestion, filtration, and subsequent centrifugation. These stromal-vascular cells were seeded on 25-cm2 tissue culture flasks and proliferated to confluency in 10% fetal bovine serum in DMEM/F12 (50:50). Cultures were differentiated using 2% pig serum + 10 mM isobutyl methylxanthine + 1 microM dexamethasone for 48 h. This medium was replaced with 5% pig serum + 1 microM insulin to promote lipid filling of adipocytes for 7 d. Adipocyte-containing cultures were incubated overnight in serum-free medium and then used for experiments. Acute experiments assessed lipolysis in cultures exposed to porcine leptin (0 to 1,000 ng/mL medium) for 2 h. Chronic experiments used cultures incubated with 100 ng porcine leptin/mL of medium for 72 h prior to lipolysis measurements. Direct effects of leptin were examined by incubating cultures in DMEM/F12, 25 mM HEPES, 3% bovine serum albumin, 20 mU of adenosine deaminase/mL of medium in the presence of 0 to 1,000 ng of porcine leptin/mL of medium. Indirect effects of leptin were examined using the same incubation medium but also supplemented with 1 microM isoproterenol +/- 10 nM insulin in the presence of 0 to 1,000 ng of porcine leptin/mL of medium. Media glycerol concentration was measured at the end of 2-h incubations. Acute leptin exposure induced up to a 76% increase in lipolysis (P < 0.05) but had no effect on insulin's inhibition of lipolysis. Chronic exposure to leptin produced up to a 56% increase in lipolysis (P < 0.05) and reduced insulin's inhibition ofisoproterenol-stimulated lipolysis by up to 31% (P < 0.05). These data demonstrate leptin functions to promote the partitioning of energy away from lipid accretion within porcine adipose tissue by promoting lipolysis directly and indirectly by reducing insulin-mediated inhibition of lipolysis.
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PMID:Porcine leptin alters insulin inhibition of lipolysis in porcine adipocytes in vitro. 1126 25