Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspartate transcarbamylase (carbamoyl-phosphate: L-aspartate carbamoyltransferase, EC 2.1.3.2) has been purified from Mycobacterium smegmatis TMC 1546 using streptomycin sulphate precipitation, ammonium sulphate precipitation, DE-52 chromatography, second ammonium sulphate precipitation, Sephadex G-200 gel filtration, and aspartate-linked CNBr-activated Sepharose 4B affinity chromatography in successive order. The enzyme was purified 231.6-fold, and the preparation was found to be homogeneous on column chromatography and polyacrylamide gel electrophoresis. The purified enzyme had a molecular weight of 246,000 and was composed of two asymmetrical subunits. The kinetic and regulatory properties of aspartate transcarbamylase from M. smegmatis were also studied. The enzyme was found to be an allosteric in nature with carbamyl phosphate showing positive cooperativity and UMP exhibiting a negative cooperativity. CTP was found to be the most potent inhibitor among nucleotides. Phosphate acted as a non-competitive product inhibitor with respect to aspartate. Succinate and maleate exerted a competitive inhibition when aspartate was the variable substrate.
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PMID:Purification and properties of aspartate transcarbamylase from Mycobacterium smegmatis. 334 42

Two approaches are used to assess publication bias in the environmental tobacco smoke/coronary heart disease (ETS/CHD) literature: (1) Statistical tests applied to all sex-specific relative risk (rr) estimates from 14 previously published studies indicate that publication bias is likely. A funnel graph of the studies' log relative risks plotted against their standard errors is asymmetrical, and weighted regression of the studies' log relative risks on their standard errors is significant (P < 0.01). (2) Previously unpublished ETS/CHD relative risks from the American Cancer Society's Cancer Prevention Studies (CPS-I and CPS-II) and the National Mortality Followback Survey (NMFS) do not show an increased CHD risk associated with ETS exposure. CPS-I: men, rr = 0.97 (0.90-1.05); CPS-I: women, rr = 1.03 (0.98-1.08); CPS-II: men, rr = 0.97 (0.87-1.08); CPS-II: women, rr = 1.00, (0.88-1.14); NMFS: men, rr = 0.97 (0.73-1.28); women, rr = 0.99 (0.84-1.16). Comparison of pooled relative risk estimates from 14 previously published studies (rr = 1.29; 1.18-1.41) and unpublished results from three studies (rr = 1.00; 0.97-1.04) also indicates that published data overestimate the association of spousal smoking and CHD (chi 2 = 25.1; P < 0.0001).
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PMID:Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. 778 30