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21.
S J Friedberg S T Weintraub D Peterson N Satsangi 《Biochemical and biophysical research communications》1987,145(3):1177-1184
We have previously provided evidence for a mechanism by which acyl DHAP is converted enzymatically to O-alkyl DHAP. This mechanism involves, in part, the formation of an endiol of acyl DHAP, loss of the fatty acid by splitting of the DHAP carbon-1 to oxygen bond and the gain of a long chain fatty alcohol. It has been shown that acyl DHAP can exchange its fatty acid for one in the medium, presumably by the mediation of O-alkyl DHAP synthase. In the present investigation we have shown that the fatty acid which is gained by acyl DHAP in the exchange process retains both carboxyl oxygens, as predicted by our postulated mechanism. This reaction is exceptional because the usual action of acyl hydrolases is to cleave at the oxygen to acyl bond. 相似文献
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Some physiological characteristics of a mutant (E1) of Anacystis nidulans R2, incapable of growing at air level of CO2, are described. E1 is capable of accumulating inorganic carbon (Ci) internally as efficiently as the wild type (R2). The apparent photosynthetic affinity for Ci in E1, however, is some 1000 times lower than that of R2. The kinetic parameters of ribulose 1,5-bisphosphate carboxylase/oxygenase from E1 are similar to those observed in R2. The mutant appears to be defective in its ability to utilize the intracellular Ci pool for photosynthesis and depends on extracellular supply of Ci in the form of CO2. The very high apparent photosynthetic Km (CO2) of the mutant indicate a large diffusion resistance for CO2. Data obtained here are used to calculate the permeability coefficient for CO2 between the bulk medium and the carboxylation site of cyanobacteria. 相似文献
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Wickliffe JK Herring SM Hallberg LM Galbert LA Masters OE Ammenheuser MM Xie J Friedberg EC Lloyd RS Abdel-Rahman SZ Ward JB 《Chemico-biological interactions》2007,166(1-3):226-231
1,3-Butadiene (BD) is a well-documented mutagen and carcinogen in rodents and is currently classified as a probable carcinogen in humans. Studies investigating workers exposed to BD indicate that, in some plants, there may be an increased genetic risk, and that polymorphisms in biotransformation and DNA repair proteins may modulate genetic susceptibility. To investigate the role of genetic polymorphisms in microsomal epoxide hydrolase (mEH) or nucleotide excision repair (NER) in contributing to the mutagenicity of BD, we conducted a series of experiments in which mice lacking mEH or NER activity were exposed to BD by inhalation or to the reactive epoxide metabolites of BD (epoxybutene-EB or diepoxybutane-DEB) by i.p. injection. Genetic susceptibility was measured using the Hprt cloning assay. Both deficient strains of mouse were significantly more sensitive to the mutagenic effects of BD and the injected epoxides. These studies provide support for the critical role that mEH plays in the biotransformation of BD, and the role that NER plays in maintaining genomic integrity following exposure to BD. Additional studies are needed to examine the importance of base excision repair (BER) in maintaining genomic integrity, the differential formation of DNA and protein adducts in deficient strains, and the potential for enhanced sensitivity to BD genotoxicity in mice either lacking or deficient in both biotransformation and DNA repair activity. 相似文献
26.
Friedberg I Nika K Tautz L Saito K Cerignoli F Friedberg I Godzik A Mustelin T 《FEBS letters》2007,581(13):2527-2533
A novel human dual-specific protein phosphatase (DSP), designated DUSP27, is here described. The DUSP27 gene contains three exons, rather than the predicted 4-14 exons, and encodes a 220 amino acid protein. DUSP27 is structurally similar to other small DSPs, like VHR and DUSP13. The location of DUSP27 on chromosome 10q22, 50 kb upstream of DUSP13, suggests that these two genes arose by gene duplication. DUSP27 is an active enzyme, and its kinetic parameters and were determined. DUSP27 is a cytosolic enzyme, expressed in skeletal muscle, liver and adipose tissue, suggesting its possible role in energy metabolism. 相似文献
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Xeroderma pigmentosum (XP) genetic complementation group C (XP-C) is the most common form of the disease worldwide. Thirty-four distinct genetic defects have been identified in 45 XP-C patients. Further identification of such defects and the frequency of their occurrence offers the potential of generating diagnostic and prognostic molecular screening panels. Archival material (such as formalin-fixed paraffin embedded skin) may be useful for the identification of novel genetic variations and for documenting the frequency of individual genetic defects in patients who are no longer available for study. However, the use of archival material precludes direct analysis of changes in the mRNA resulting from genomic changes. The serendipitous reacquisition of an XP individual in whom genetic defects were previously characterized in archival material allowed confirmation of the defects as well as a direct analysis of the consequences of these defects on mRNA, mRNA expression and on cellular phenotypes. 相似文献
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Ingrid van der Pluijm George A Garinis Renata M. C Brandt Theo G. M. F Gorgels Susan W Wijnhoven Karin E. M Diderich Jan de Wit James R Mitchell Conny van Oostrom Rudolf Beems Laura J Niedernhofer Susana Velasco Errol C Friedberg Kiyoji Tanaka Harry van Steeg Jan H. J Hoeijmakers Gijsbertus T. J van der Horst 《PLoS biology》2007,5(1)
29.
The field of DNA damage responsiveness in general, and the consequences of endogenous and exogenous base damage in DNA, in particular, has made new and exciting contributions to our increasing understanding of the initiation and progression of neoplasia in humans. This article presents some of the highlights in this area of investigation, with a particular emphasis on DNA repair, the tolerance of DNA damage and its contribution to mutagenesis, and DNA damage checkpoint regulation. 相似文献
30.
Achieving the goals of structural genomics initiatives depends on the outcomes of two groups of factors: the number and distribution of experimentally determined protein structures, and our ability to assign novel proteins to known structures (fold recognition) and use them to build models (modeling). The quality of the tools used for fold recognition defines the scope of experimental effort - the more distant the templates that can be recognized, the smaller the number of proteins that have to be solved. Recent improvements in fold recognition may have suggested that the goals of structural genomics initiatives are getting closer. However, problems that surfaced during the first few years of active work have put many of the early estimates in doubt and new ones are still slow in coming. 相似文献