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Damaged Sites (damaged + site)
Selected AbstractsAt the birth of molecular radiation biology ,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2-3 2001Raymond Devoret Abstract Rational thinking builds on feelings, too. This article starts with a tribute to Richard Setlow, an eminent scientist; it retraces as well some studies in molecular genetics that helped to understand basic questions of radiation biology. In the mid-1950s, the induction of a dormant virus (prophage) by irradiation of its host was an intriguing phenomenon. Soon, it was found that prophage induction results from the inactivation of the prophage repressor. Similarly, a score of induced cellular SOS functions were found to be induced when the LexA repressor is inactivated. Repressor inactivation involves the formation of a newly formed distinctive structure: a RecA-polymer wrapped around single-stranded DNA left by the arrest of replication at damaged sites. By touching this RecA nucleofilament, the LexA repressor is inactivated, triggering the sequential expression of SOS functions. The RecA nucleofilament acts as a chaperone, allowing recombinational repair to occur after nucleotide excision repair is over. The UmuD,C complex, synthesized slowly and parsimoniously, peaks at the end of recombinational repair, ready to be positioned at the tip of a RecA nucleofilament, placing the UmuD,C complex right at a lesion. At this location, UmuD,C prevents recombinational repair, and now acts as an error-prone paucimerase that fills the discontinuity opposite the damaged DNA. Finally, the elimination of lesions from the path of DNA polymerase, allows the resumption of DNA replication, and the SOS repair cycle switches to a normal cell cycle. Environ. Mol. Mutagen. 38:135,143, 2001. © 2001 Wiley-Liss, Inc. [source] A Facile Strategy for Preparing Self-Healing Polymer Composites by Incorporation of Cationic Catalyst-Loaded Vegetable FibersADVANCED FUNCTIONAL MATERIALS, Issue 14 2009Ding Shu Xiao Abstract A two-component healing agent, consisting of epoxy-loaded microcapsules and an extremely active catalyst (boron trifluoride diethyl etherate, (C2H5)2O,·,BF3)), is incorporated into epoxy composites to provide the latter with rapid self-healing capability. To avoid deactivation of the catalyst during composite manufacturing, (C2H5)2O,·,BF3 is firstly absorbed by fibrous carriers (i.e., short sisal fibers), and then the fibers are coated with polystyrene and embedded in the epoxy matrix together with the encapsulated epoxy monomer. Because of gradual diffusion of the absorbed (C2H5)2O,·,BF3 from the sisal into the surrounding matrix, the catalyst is eventually distributed throughout the composites and acts as a latent hardener. Upon cracking of the composites, the epoxy monomer is released from the broken capsules, spreading over the cracked planes. As a result, polymerization, triggered by the dispersed (C2H5)2O,·,BF3, takes place and the damaged sites are rebonded. Since the epoxy,BF3 cure belongs to a cationic chain polymerization, the exact stoichiometric ratio of the reaction components required by other healing chemistries is no longer necessary. Only a small amount of (C2H5)2O,·,BF3 is sufficient to initiate very fast healing (e.g., a 76% recovery of impact strength is observed within 30,min at 20,°C). [source] Direct Visualization of Abasic Sites on a Single DNA Molecule Using Fluorescence Microscopy,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2002Tamaki Hirose ABSTRACT A new method was developed to allow direct visualization of damaged sites on individual DNA molecules. Fluorescence in situ hybridization on extended DNA molecules was modified to detect a single abasic site. Abasic sites were specifically labeled with a biotinylated aldehyde-reactive probe and fluorochrome-conjugated streptavidin. The light emitted by a single fluorochrome,DNA complex was calibrated. The number of abasic sites on the DNA molecule was estimated by counting each fluorochrome,DNA complex. The present study directly visualized and characterized the abasic sites of single DNA molecules. [source] Bound Transcription Factor Suppresses Photoproduct Formation in the NF-,B Promoter,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2001Rita Ghosh ABSTRACT The relationship between purified transcription factor p50 binding and ultraviolet light,induced DNA damage formation in the NF-,B promoter element was investigated. The effect of bound transcription factor on cyclobutane dimer formation was quantified using Maxam,Gilbert analysis of irradiated substrate digested with T4 phage endonuclease V. Two methods were employed for cleaving (6-4) photoproducts. Sites of (6-4) photoproducts cleaved by piperidine showed a general suppression in the presence of bound p50 protein similar to that observed for cyclobutane dimers. In contrast to piperidine, digestion with ultraviolet damage endonuclease (UVDE) from Saccharomyces pombe subsequent to cyclobutane dimer reversal by photolyase displayed a broader spectrum of damaged sites. Whereas some of these sites were suppressed by bound p50 protein, some remained unaffected and one site showed increased (6-4) photoproduct induction. These data illustrate the advantage of UVDE over piperidine for studying (6-4) photoproducts at the sequence level and suggest that this approach may be useful for footprinting transcription factor binding in other promoters. [source] | ||||||||||