Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have identified two types of polymorphism at the CAR (cell adhesion regulator) locus. One is a conventional TaqI polymorphism and the other is an insertion/deletion polymorphism in the coding region. One has the nucleotide sequence AGTGAGGCA (Ser-Gln-Ala) at nt 271-279, whereas the variant has ACAC-AGTGAGGCCCA (Thr-Gln-Ser-Gly-Pro). Although it is not clear whether this variation of amino acids affects the biological function of the gene product, this variant was detected in nine chromosomes among 30 unrelated Japanese individuals. Genetic linkage analysis based on the genotypes of TaqI polymorphism in CEPH families revealed close linkage of CAR to D16S7 and D16S154, which are located in the peritelomeric region of the long arm of chromosome 16.
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PMID:The cell adhesion regulator (CAR) gene, TaqI and insertion/deletion polymorphisms, and regional assignment to the peritelomeric region of 16q by linkage analysis. 809 8

Clinical and experimental data have recently accumulated for antithrombotic action of angiotensin-converting enzyme inhibitors (ACE-1s). We have shown previously that captopril (which contains a thiol group in the moiety) exerts more pronounced antithrombotic activity than does an equipotent dose of enalapril (the drug devoid of the thiol group). To clarify the relative importance of the presence of the thiol group in the molecule versus angiotensin-converting enzyme (ACE) inhibitory properties in the antithrombotic action of captopril, rats were treated with captopril (5 mg/kg twice daily; CAP), epicaptopril (stereoisomer of captopril devoid of ACE-inhibitory properties; 5 mg/kg twice daily; EPI), N-acetylcysteine (3.75 mg/kg twice daily; ACC), enalapril (3 mg/kg once daily; ENA), or distilled water (VEH) for 10 days, per os. After ligation of the vena cava, the incidence of the venous thrombosis and/or the thrombus weight decreased significantly in all but the ENA-treated groups when compared with control rats. The effect of CAP, EPI, and ACC was accompanied by a marked reduction of euglobulin clot lysis time and, with the exception of ACC, by an increase in prothrombin time in the blood collected from the site of the thrombus formation. Antithrombotic activity of EPI was completely abolished by nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) or indomethacin, with the parallel reversal of fibrinolytic and coagulation parameters toward normal. Activated partial thromboplastin time, mean blood pressure, and bleeding time were not altered by either of the administered drugs. Thus, we demonstrated that thiol compounds exert antithrombotic activity by increasing fibrinolysis and/or suppression of the extrinsic pathway of the coagulation cascade in a nitric oxide/prostacyclin-dependent manner.
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PMID:Thiol repletion prevents venous thrombosis in rats by nitric oxide/prostacyclin-dependent mechanism: relation to the antithrombotic action of captopril. 1102 53

We sequenced all nine exons, exon-intron junctions including a part of introns, 5'-flanking and 3'-untranslated regions of the cytochrome P450 (CYP) 2A13 gene from 192 Japanese individuals. We found eighteen novel genetic polymorphisms including five single nucleotide polymorphisms (SNP) and one three base pair insertion causing amino acid substitution and one amino acid insertion, respectively, one silent SNP in exon 4, four SNPs in a 5'-flanking region, and seven SNPs in introns. The five SNPs (74G>A in exon 1, 579G>A in exon 2, 1706C>G in exon 3, and 7343T>A and 7465C>T in exon 9) causing amino acid substitutions (Arg(25)Gln, Arg(101)Gln, Asp(158)Glu, Phe(453)Tyr, and Arg(494)Cys), respectively. The one three base pair insertion (1634_1635 ACC insertion in exon 3) caused one amino acid insertion ((133_134)Thr ins). These sequences are as follows:SNP, 021125Fujieda005; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base;5'-TGTCAGTCTGGCG/AGCAGAGGAAGAG-3'.SNP, 021125Fujieda007; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base; 5'-AGTTCAGCGGGCG/AAGGCGAGCAGGC-3'.SNP, 021125Fujieda009; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base; 5'-CTTCCTCATCGAC/GGCCCTCCGGGGC-3'.SNP, 021125Fujieda017; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base; 5'-TCTTTCTCTTCTT/ACACCACCATCAT-3'.SNP, 021125Fujieda018; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base; 5'-AGCTTCCTGCCCC/TGCTGAGCGAGGG-3'.SNP, 021125Fujieda008; GENE NAME, CYP2A13; ACCESSION NUMBER, NG_000008; LENGTH, 25 base; 5'-CTCCATCGCCACC-/ACCCTAAGGGGTTTT-3'.
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PMID:Eighteen novel polymorphisms of the CYP2A13 gene in Japanese. 1561 22

The cortisol rise after awakening (cortisol awakening response, CAR) is a core biomarker of hypothalamic-pituitary-adrenal (HPA) axis regulation related to psychosocial stress and stress-related psychiatric disorders. However, the neural regulation of the CAR has not been examined in humans. Here, we studied neural regulation related to the CAR in a sample of 25 healthy human participants using an established psychosocial stress paradigm together with multimodal functional and structural (voxel-based morphometry) magnetic resonance imaging. Across subjects, a smaller CAR was associated with reduced grey matter volume and increased stress-related brain activity in the perigenual ACC, a region which inhibits HPA axis activity during stress that is implicated in risk mechanisms and pathophysiology of stress-related mental diseases. Moreover, functional connectivity between the perigenual ACC and the hypothalamus, the primary controller of HPA axis activity, was associated with the CAR. Our findings provide support for a role of the perigenual ACC in regulating the CAR in humans and may aid future research on the pathophysiology of stress-related illnesses, such as depression, and environmental risk for illnesses such as schizophrenia.
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PMID:Neural Correlates of the Cortisol Awakening Response in Humans. 2578 Dec 68

Stunting, chlorosis, and light yellow mottling resembling symptoms of nutrient deficiency were observed in angelonia (Angelonia angustifolia) in commercial production in New York. Numerous, filamentous particles 520 to 540 nm long and spherical virus particles 30 nm in diameter were observed by transmission electron microscopy (TEM) in negatively stained partially purified extracts of symptomatic Angelonia leaf tissue. Two viruses, the filamentous potexvirus Alternanthera mosaic virus (AltMV) and the spherical carmovirus Angelonia flower break virus (AnFBV) were subsequently identified on the basis of nucleotide sequence analysis of amplicons generated by reverse transcription (RT)-PCR using total RNA isolated from infected leaf tissue. A 584-bp portion of the replicase-encoding region of the AltMV genome was obtained with the degenerate primers Potex 2RC (5'-AGC ATR GNN SCR TCY TG-3') and Potex 5 (5'-CAY CAR CAR GCM AAR GAT GA-3') (3). Forward (AnFBV CP 1F-5'-AGC CTG GCA ATC TGC GTA CTG ATA-3') and reverse (AnFBV CP 1R-5'-AAT ACC GCC CTC CTG TTT GGA AGT-3') primers based on the published AnFBV genomic sequence (GenBank Accession No. NC_007733) were used to amplify a portion of the viral coat protein (CP) gene. The nucleotide sequence of the amplicon generated using the potexvirus-specific primers (GenBank Accession No. EU679362) was 99% identical to the published AltMV (GenBank Accession No. NC_007731) sequence and the nucleotide sequence of the amplicon obtained using the AnFBV CP primers was 99% identical to the published AnFBV genomic sequence (GenBank Accession No. EU679363). AnFBV occurs widely in angelonia (1) and AltMV has been identified in phlox (2). These data confirm the presence of AltMV and AnFBV in diseased angelonia plants showing stunting and nutrient deficiency-like symptoms and substantiates, to our knowledge, this first report of AltMV in angelonia in the United States. References: (1) S. Adkins et al. Phytopathology 96:460, 2006. (2) J. Hammond et al. Arch. Virol. 151:477, 2006. (3) R. A. A. van der Vlugt and M. Berendeson. Eur. J. Plant Pathol. 108:367, 2002.
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PMID:First Report of Alternanthera mosaic virus Infection in Angelonia in the United States. 3076 47