Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 21 to 27 of 27

Publication Record

Connections

Regulation of serotonin-2C receptor G-protein coupling by RNA editing.
Burns CM, Chu H, Rueter SM, Hutchinson LK, Canton H, Sanders-Bush E, Emeson RB
(1997) Nature 387: 303-8
MeSH Terms: 3T3 Cells, Adenosine, Adenosine Deaminase, Animals, Binding, Competitive, Brain, Cell Line, Choroid Plexus, Corpus Striatum, GTP-Binding Proteins, Hippocampus, Humans, Inosine, Mice, RNA Editing, RNA, Messenger, RNA-Binding Proteins, Rats, Receptor, Serotonin, 5-HT2C, Receptors, Serotonin, Serotonin, Signal Transduction, Transfection, Tumor Cells, Cultured
Show Abstract · Added July 12, 2010
The neurotransmitter serotonin (5-hydroxytryptamine, 5-HT) elicits a wide array of physiological effects by binding to several receptor subtypes. The 5-HT2 family of receptors belongs to a large group of seven-transmembrane-spanning G-protein-coupled receptors and includes three receptor subtypes (5-HT2A, 5-HT(2B) and 5-HT(2C)) which are linked to phospholipase C, promoting the hydrolysis of membrane phospholipids and a subsequent increase in the intracellular levels of inositol phosphates and diacylglycerol. Here we show that transcripts encoding the 2C subtype of serotonin receptor (5-HT(2C)R) undergo RNA editing events in which genomically encoded adenosine residues are converted to inosines by the action of double-stranded RNA adenosine deaminase(s). Sequence analysis of complementary DNA isolates from dissected brain regions have indicated the tissue-specific expression of seven major 5-HT(2C) receptor isoforms encoded by eleven distinct RNA species. Editing of 5-HT(2C)R messenger RNAs alters the amino-acid coding potential of the predicted second intracellular loop of the receptor and can lead to a 10-15-fold reduction in the efficacy of the interaction between receptors and their G proteins. These observations indicate that RNA editing is a new mechanism for regulating serotonergic signal transduction and suggest that this post-transcriptional modification may be critical for modulating the different cellular functions that are mediated by other members of the G-protein-coupled receptor superfamily.
1 Communities
1 Members
0 Resources
24 MeSH Terms
Winner of the Theodore E. Woodward Award: c-Myb and the coordinate regulation of thymic genes.
Hutton JJ, Ess KC, Witte DP, Aronow BJ
(1996) Trans Am Clin Climatol Assoc 107: 115-24
MeSH Terms: Adenosine Deaminase, Animals, Awards and Prizes, Base Sequence, DNA, Embryonic and Fetal Development, Gene Expression Regulation, Developmental, Hematopoiesis, Humans, Molecular Sequence Data, Oncogenes, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-myb, RNA, Messenger, Societies, Medical, Thymus Gland, Trans-Activators, United States
Added June 9, 2010
0 Communities
1 Members
0 Resources
18 MeSH Terms
Activation of metabotropic glutamate receptors increases cAMP accumulation in hippocampus by potentiating responses to endogenous adenosine.
Winder DG, Conn PJ
(1993) J Neurosci 13: 38-44
MeSH Terms: Adenosine, Adenosine Deaminase, Animals, Cyclic AMP, Cycloleucine, Drug Synergism, Hippocampus, In Vitro Techniques, Male, Rats, Rats, Sprague-Dawley, Receptors, Glutamate, Receptors, Purinergic
Show Abstract · Added May 19, 2014
Metabotropic glutamate receptors (mGluRs) are coupled to effector systems through GTP-binding proteins (G-proteins) and appear to mediate slow synaptic responses in the CNS. Although mGluR-mediated increases in phosphoinositide hydrolysis have been well characterized, other mechanisms for signal transduction employed by mGluRs are poorly understood. We recently reported that the selective mGluR agonist 1-aminocyclopentane-1 S,3R-dicarboxylic acid (1S,3R-ACPD) increases cAMP accumulation in rat hippocampal slices. We have now investigated the mechanisms involved in this response. A number of G-protein-linked receptors that are not directly coupled to adenylate cyclase increase cAMP accumulation by potentiating cAMP responses to other agonists. Furthermore, previous studies suggest that glutamate increases cAMP accumulation by a mechanism that is dependent upon the presence of endogenous adenosine. Therefore, we tested the hypothesis that 1S,3R-ACPD-stimulated increases in cAMP accumulation in rat hippocampal slices are dependent upon the presence of endogenous adenosine and are mediated by an mGluR that potentiates cAMP responses to other agonists. We found that adenosine deaminase abolished 1S,3R-ACPD-stimulated cAMP accumulation whereas the adenosine uptake blocker dipyridamole enhanced this response. Additionally, adenosine receptor antagonists blocked mGluR-mediated increases in cAMP accumulation with potencies that were highly correlated with their potencies at A2 adenosine receptors. Furthermore, we performed a series of studies that suggest that 1S,3R-ACPD activates an mGluR subtype that potentiates responses to agonists of other receptors that are coupled to adenylate cyclase and that 1S,3R-ACPD-stimulated increases in cAMP accumulation in hippocampal slices are mediated by potentiation of the cAMP response to low levels of endogenous adenosine that are continuously present extracellularly.
0 Communities
2 Members
0 Resources
13 MeSH Terms
Double-stranded phosphorothioate oligonucleotide modulation of gene expression.
Ess KC, Hutton JJ, Aronow BJ
(1994) Ann N Y Acad Sci 716: 321-3
MeSH Terms: Adenosine Deaminase, Cell Line, Enhancer Elements, Genetic, Gene Expression, Humans, Oligonucleotides, T-Lymphocytes
Added June 9, 2010
0 Communities
1 Members
0 Resources
7 MeSH Terms
A central role for a single c-Myb binding site in a thymic locus control region.
Ess KC, Whitaker TL, Cost GJ, Witte DP, Hutton JJ, Aronow BJ
(1995) Mol Cell Biol 15: 5707-15
MeSH Terms: Adenosine Deaminase, Animals, Base Sequence, Binding Sites, Cell Line, Chromatin, Enhancer Elements, Genetic, Gene Expression Regulation, Developmental, Humans, Introns, Mice, Mice, Transgenic, Molecular Sequence Data, Point Mutation, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-myb, Saccharomyces cerevisiae, T-Lymphocytes, Thymus Gland, Trans-Activators
Show Abstract · Added June 9, 2010
Locus control regions (LCRs) are powerful assemblies of cis elements that organize the actions of cell-type-specific trans-acting factors. A 2.3-kb LCR in the human adenosine deaminase (ADA) gene first intron, which controls expression in thymocytes, is composed of a 200-bp enhancer domain and extended flanking sequences that facilitate activation from within chromatin. Prior analyses have demonstrated that the enhancer contains a 28-bp core region and local adjacent augmentative cis elements. We now show that the core contains a single critical c-Myb binding site. In both transiently cotransfected human cells and stable chromatin-integrated yeast cells, c-Myb strongly transactivated reporter constructs that contained polymerized core sequences. c-Myb protein was strongly evident in T lymphoblasts in which the enhancer was active and was localized within discrete nuclear structures. Fetal murine thymus exhibited a striking concordance of endogenous c-myb expression with that of mouse ADA and human ADA LCR-directed transgene expression. Point mutation of the c-Myb site within the intact 2.3-kb LCR severely attenuated enhancer activity in transfections and LCR activity in transgenic thymocytes. Within the context of a complex enhancer and LCR, c-Myb can act as an organizer of thymocyte-specific gene expression via a single binding site.
0 Communities
1 Members
0 Resources
20 MeSH Terms
Metabolic and functional consequences of inhibiting adenosine deaminase during renal ischemia in rats.
Stromski ME, van Waarde A, Avison MJ, Thulin G, Gaudio KM, Kashgarian M, Shulman RG, Siegel NJ
(1988) J Clin Invest 82: 1694-9
MeSH Terms: Adenosine Deaminase Inhibitors, Adenosine Triphosphate, Animals, Coformycin, Inulin, Ischemia, Kidney, Magnetic Resonance Spectroscopy, Male, Nucleoside Deaminases, Pentostatin, Rats, Rats, Inbred Strains
Show Abstract · Added December 10, 2013
The concentrations of renal ATP have been measured by 31P-nuclear magnetic resonance (NMR) before, during, and after bilateral renal artery occlusion. Using in vivo NMR, the initial postischemic recovery of ATP increased with the magnitude of the residual nucleotide pool at the end of ischemia. ATP levels after 120 min of reflow correlated with functional recovery at 24 h. In the present study the effect of blocking the degradation of ATP during ischemia upon the postischemic restoration of ATP was investigated. Inhibition of adenosine deaminase by 80% with the tight-binding inhibitor 2'-deoxycoformycin led to a 20% increase in the residual adenine nucleotide pool. This increased the ATP initial recovery after 45 min of ischemia from 52% (in controls) to 62% (in the treated animals), as compared to the basal levels. The inhibition also caused an accelerated postischemic restoration of cellular ATP so that at 120 min it was 83% in treated rats vs. 63% in untreated animals. There was a corresponding improvement in the functional recovery from the insult (increase of 33% in inulin clearance 24 h after the injury). Inhibition of adenosine deaminase during ischemia results in a injury similar to that seen after a shorter period of insult.
0 Communities
1 Members
0 Resources
13 MeSH Terms
Gene for non-insulin-dependent diabetes mellitus (maturity-onset diabetes of the young subtype) is linked to DNA polymorphism on human chromosome 20q.
Bell GI, Xiang KS, Newman MV, Wu SH, Wright LG, Fajans SS, Spielman RS, Cox NJ
(1991) Proc Natl Acad Sci U S A 88: 1484-8
MeSH Terms: Adenosine Deaminase, Chromosomes, Human, Pair 20, DNA, Diabetes Mellitus, Type 2, Female, GTP-Binding Proteins, Genetic Linkage, Humans, Male, Pedigree, Polymorphism, Genetic, Recombination, Genetic
Show Abstract · Added February 22, 2016
Maturity-onset diabetes of the young (MODY) is a form of non-insulin-dependent diabetes mellitus characterized by an early age of onset, usually before 25 years of age, and an autosomal dominant mode of inheritance. The largest and best-studied MODY pedigree is the RW family. The majority of the diabetic subjects in this pedigree has a reduced and delayed insulin-secretory response to glucose, and it has been proposed that this abnormal response is the manifestation of the basic genetic defect that leads to diabetes. Using DNA from members of the RW family, we tested more than 75 DNA markers for linkage with MODY. A DNA polymorphism in the adenosine deaminase gene (ADA) on the long arm of chromosome 20 was found to cosegregate with MODY. The maximum logarithm of odds (lod score) for linkage between MODY and ADA was 5.25 at a recombination fraction of 0.00. These results indicate that the odds are greater than 178,000:1 that the gene responsible for MODY in this family is tightly linked to the ADA gene on chromosome 20q.
0 Communities
1 Members
0 Resources
12 MeSH Terms