![]() ![]() Among the highlights are excellent coverage of both base excision repair (BER) and nucleotide excision repair (NER), useful assays for identifying and quantifying UV-induced DNA lesions and DNA breakage, gene therapy, environmental mutagenesis and cancer, and gene targeting. The authors address a broad range of questions about practical mammalian DNA repair, including such arcana as 'what is radioresistant DNA synthesis and how is it measured?' The techniques presented are readily reproducible and offer cutting-edge methods for cytogenetic analysis, measuring the cellular response to ionizing radiation, detecting single-strand (nicks) and double-strand DNA breaks, detecting the presence of 'adducted' bases in DNA, and preparing mismatch repair (MMR) plasmid substrates. Thus, the knowledge of apoptotic and survival pathways activated in tumor cells may help in establishing specific therapies by combining selective inhibitors or stimulators of key signaling proteins with conventional chemotherapy, hormone therapy, and radiotherapy.Henderson has refocused the book on mammalian cells, adding fourteen entirely new chapters and extensively revising many of the remaining chapters. Moreover, the presence of viable cells up to 7 days in samples exposed to 6 Gy is explained by Akt activation, which may influence the nuclear transcription factor CREB, leading to resistance to ionizing radiation. The response was apparently promoted by caspase-3-mediated PKCδ activation, and thus apoptosis. This arrest was accompanied by dead cells, which increased in number up to 7 days, when cell viability was further reduced. Cell cycle analysis, performed by flow cytometry, showed a significant G2M arrest 24 h after exposure to 6 Gy. Here we report the effect of 1.5- and 6-Gy doses of ionizing radiation on apoptotic protein kinase Cδ (PKCδ) and survival cyclic-nucleotide response element-binding protein (CREB) signal in Jurkat T cells. Although ionizing radiation induces a loss of proliferative capacity as well as cell death by apoptosis and necrosis, cells can oppose the damaging effects by activating survival signal pathways. ![]()
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