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排序方式: 共有177条查询结果,搜索用时 15 毫秒
1.
Reconstitution of RecBC DNase activity from purified Escherichia coli RecB and RecC proteins 总被引:8,自引:0,他引:8
I D Hickson C N Robson K E Atkinson L Hutton P T Emmerson 《The Journal of biological chemistry》1985,260(2):1224-1229
The Escherichia coli RecB protein, normally synthesized in low amounts, has been amplified by linkage of the recB gene to the phage lambda leftward promoter in an expression plasmid. From strains harboring this plasmid, RecB protein has been purified to homogeneity by a simple procedure which includes affinity chromatography on a column of RecC protein bound to agarose. The purified RecB protein has DNA-dependent ATPase activity but no exonuclease activity. RecC protein alone has neither ATPase nor exonuclease activity. However, when combined together, the RecB and RecC proteins show the ATP-dependent double-stranded exonuclease properties characteristic of the RecBC DNase. 相似文献
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Hypoxanthine-guanine phosphoribosyltransferase (HPRT, EC 2.4.2.8) is a purine salvage enzyme that catalyses the conversion of hypoxanthine and guanine to their respective mononucleotides. Partial deficiency of this enzyme can result in the overproduction of uric acid leading to a severe form of gout, whilst a virtual absence of HPRT activity causes the Lesch-Nyhan syndrome which is characterised by hyperuricaemia, mental retardation, choreoathetosis and compulsive self-mutilation. The HPRT-encoding gene is located on the X chromosome in the region q26–q27 and consists of nine exons and eight introns totalling 57 kb. This gene is transcribed to produce an mRNA of 1.6 kb, which contains a protein encoding region of 654 nucleotides. With the advent of increasingly refined techniques of molecular biology, it has been possible to study the HPRT gene of individuals with a deficiency in HPRT activity to determine the genetic basis of the enzyme deficiency. Many different mutations throughout the coding region have been described, but in the absence of precise information on the three-dimensional structure of the HPRT protein, it remains difficult to determine any consistent correlation between the structure and function of the enzyme. 相似文献
4.
Genotoxicity studies on the preemergence herbicide trifluralin 总被引:4,自引:0,他引:4
M L Garriott E R Adams G S Probst J L Emmerson T J Oberly D E Kindig S B Neal B J Bewsey M A Rexroat 《Mutation research》1991,260(2):187-193
5.
Experiments were conducted using twin-well calorimetry to determine the averaged whole-body specific absorption rate (SAR) for rat carcasses exposed to 360, 700, 915, and 2,450 MHz CW radiation in an anechoic chamber. All exposures were done with the long axis of the rat in an E-polarization. Additional experiments were conducted using a fiber optical temperature probe to determine local SAR in the brain, esophagus, colon, rectum, and tail during microwave exposure. The whole-body averaged SAR for the radiation frequencies examined follows a nonmonotonic function with 700 MHz as the resonant frequency. This result agrees with previous analytical estimates. Local SARs within the body and tail are nonuniform with significant frequency-specific hotspots in the colon, rectum, and tail. 相似文献
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Summary Protein X, molecular weight 40,000, has been separated from the other proteins of E. coliby a two-dimensional gel electrophoretic technique which separates proteins according to isoelectric point (pI) in the firstdimension and according to molecular weight in the second. When protein X is induced in wild-type cells by mitomycin C treatmentit has a pI6.0. However, when protein X is induced in a tif-1 mutant, either by temperatureshift-up to 42° or by mitomycin C treatment at 30°, it has a pI6.2. The low level of protein X which is present inuninduced tif mutants at 30° also has a pI6.2. These results suggest thattif-1 is a mis-sense mutation in the gene coding for protein X. Since transduction andcomplementation studies indicate that tif-1 is a mutation of therecA
+
gene (Castellazzi, Morand, George and Buttin, 1977) it follows that protein X is the recA
+ gene product.A model has been formulated to account for the relationship between protein X synthesis and the recA
+
and lexA
+
genes. In this model, a repressor coded by lexA
+
binds to the operator of the recA
+
gene from whence it can normally only be removed by the combined action of an inducer and protein X, the recA
+ product. Thus, protein X controls its own synthesis. The tif-1 mutation leads to a temperature sensitive form of protein X which, at 42°, can spontaneously remove the repressor without the intervention of the inducer. 相似文献
8.
Magnesium-induced inner membrane aggregation in heart mitochondria: prevention and reversal by carboxyatractyloside and bongkrekic acid
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Mg(2+) at an optimal concentration of 2mM (ph 6.5) induces large increases (up to 30 percent) in the optical density of bovine heart mitochondria incubated under conditions of low ionic strength (< approx. 0.01). The increases are associated with aggregation (sticking together) of the inner membranes and are little affected by changes in the energy status of the mitochondria. Virtually all of a number of other polyvalent cations tested and Ag(+) induce increases in mitochondrial optical density similar to those induced by Mg(2+), their approximate order of concentration effectiveness in respect to Mg(2+) being: La(3+) > Pb(2+) = Cu(2+) > Cd(2+) > Zn(2+) > Ag(+) > Mn(2+) > Ca(2+) > Mg(2+). With the exception of Mg(2+), all of these cations appear to induce swelling of the mitochondria concomitant with inner membrane aggregation. The inhibitors of the adenine nucleotide transport reaction carboxyatratyloside and bongkrekic acid are capable of preventing and reversing Mg(2+)-induced aggregation at the same low concentration required for complete inhibition of phosphorylating respiration, suggesting that they inhibit the aggregation by binding to the adenine nucleotide carrier. The findings are interpreted to indicate (a) that the inner mitochondrial membrane is normally prevented from aggregating by virtue of its net negative outer surface change, (b) that the cations induce the membrane to aggregate by binding at its outer surface, decreasing the net negative charge, and (c) that carboxyatractyloside and bongkrekic acid inhibit the aggregation by binding to the outer surface of the membrane, increasing the net negative charge. 相似文献
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