Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.4 (deaminase)
 5,113 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Young, Frank E. (Western Reserve University, Cleveland, Ohio). Fractionation and partial characterization of the products of autolysis of cell walls of Bacillus subtilis. J. Bacteriol. 92:839-846. 1966.-Autolysis of the cell wall of Bacillus subtilis by an indigenous autolytic enzyme results in solubilization of 90% of the cell wall. The solubilized cell wall (supernatant fraction) was fractionated by the combination of ion-exchange chromatography on diethylaminoethyl cellulose and gel filtration on Sephadex G-25 into polysaccharides (composed of N-acyl glucosamine and N-acyl muramic acid), mucopeptides, peptides, and teichoic acid. The chemical composition of the products of autolysis confirms the proposed mechanism of autolysis and establishes the autolytic enzyme as an N-acyl muramyl-l-alanine amidase. The heteropolymers in the cell wall are linked by peptide bridges. Two peptides which account for 70% of the peptides of the cell wall have a molar ratio of 1.0:0.9:1.3 for diaminopimelic acid, glutamic acid, and alanine, respectively. Other minor peptides contain diaminopimelic acid, glutamic acid, and alanine in molar ratios of 1.0:0.9:1.5, 1.0:0.5:1.0, and 1.0:1.5:1.7, respectively. The procedures employed in this study should be applicable to the fractionation of heteropolymers in cell walls of other gram-positive organisms and thereby aid in the study of the structure of antigenic determinants and endotoxins.
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PMID:Fractionation and partial characterization of the products of autolysis of cell walls of Bacillus subtilis. 495 47

Deamination of nucleobases in DNA and RNA results in the formation of xanthine (X), hypoxanthine (I), oxanine, and uracil, all of which are miscoding and mutagenic in DNA and can interfere with RNA editing and function. Among many forms of nucleic acid damage, deamination arises from several unrelated mechanisms, including hydrolysis, nitrosative chemistry, and deaminase enzymes. Here we present a fourth mechanism contributing to the burden of nucleobase deamination: incorporation of hypoxanthine and xanthine into DNA and RNA caused by defects in purine nucleotide metabolism. Using Escherichia coli and Saccharomyces cerevisiae with defined mutations in purine metabolism in conjunction with analytical methods for quantifying deaminated nucleobases in DNA and RNA, we observed large increases (up to 600-fold) in hypoxanthine in both DNA and RNA in cells unable to convert IMP to XMP or AMP (IMP dehydrogenase, guaB; adenylosuccinate synthetase, purA, and ADE12), and unable to remove dITP/ITP and dXTP/XTP from the nucleotide pool (dITP/XTP pyrophosphohydrolase, rdgB and HAM1). Conversely, modest changes in xanthine levels were observed in RNA (but not DNA) from E. coli lacking purA and rdgB and the enzyme converting XMP to GMP (GMP synthetase, guaA). These observations suggest that disturbances in purine metabolism caused by known genetic polymorphisms could increase the burden of mutagenic deaminated nucleobases in DNA and interfere with gene expression and RNA function, a situation possibly exacerbated by the nitrosative stress of concurrent inflammation. The results also suggest a mechanistic basis for the pathophysiology of human inborn errors of purine nucleotide metabolism.
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PMID:Defects in purine nucleotide metabolism lead to substantial incorporation of xanthine and hypoxanthine into DNA and RNA. 2230 25