共查询到20条相似文献,搜索用时 15 毫秒
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Tasleem Samji 《The Yale journal of biology and medicine》2009,82(4):153-159
Influenza A virus belongs to the family of Orthomyxoviridae. It is an enveloped virus with a negative sense RNA segmented genome that encodes for 11 viral genes. This virus has evolved a number of mechanisms that enable it to invade host cells and subvert the host cell machinery for its own purpose, that is, for the sole production of more virus. Two of the mechanisms that the virus uses are “cap-snatching” and preventing the host cell from expressing its own genes. This mini-review provides a brief overview as to how the virus is able to invade host cells, replicate itself, and exit the host cell. 相似文献
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The life cycle of the metazoan nuclear envelope 总被引:1,自引:0,他引:1
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The molecular control of DNA damage-induced cell death 总被引:2,自引:0,他引:2
Coultas L Strasser A 《Apoptosis : an international journal on programmed cell death》2000,5(6):491-507
Because of the singular importance of DNA for genetic inheritance, all organisms have evolved mechanisms to recognize and respond to DNA damage. In metazoans, cells can respond to DNA damage either by undergoing cell cycle arrest, to facilitate DNA repair, or by undergoing cell suicide. Cell death can either occur by activation of the apoptotic machinery or simply be a consequence of irreparable damage that prevents further cell division. In germ cells, mechanisms for limiting alterations to the genome are required for faithful propagation of the species whereas in somatic cells, responses to DNA damage prevent the accumulation of mutations that might lead to aberrant cell proliferation or behavior. Several of the genes that regulate cellular responses to DNA damage function as tumor suppressors. The clinical use of DNA damaging agents in the treatment of cancer can activate these tumor suppressors and exploits the cellular suicide and growth arrest mechanisms that they regulate. It appears that in some but not all types of tumors the propensity to undergo apoptosis is a critical determinant of their sensitivity to anti-cancer therapy. This review describes current understanding of the molecular control of DNA damage-induced apoptosis with particular attention to its role in tumor suppression and cancer therapy. 相似文献
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Izawa M Mori T Satoh T Teramachi K Sairenji T 《Apoptosis : an international journal on programmed cell death》1999,4(5):321-325
Overcoming apoptosis resistance to chemotherapy and radiation may lead to a reduction in gastric cancer death. We hypothesize that the apoptotic machinery in gastric cancer cells is dependent upon specific cellular conditions. In the course of our study of the expression of apoptosis-related genes in human gastric cancer cell lines, we have identified a cDNA clone which predicts an alternative form of caspase-9. The caspase-9 variant, which we designated as caspase-9 beta, retained a truncated structure of native caspase-9 without its catalytic domain and was expressed in seven cell lines from human gastric cancer. Among the cell lines examined, MKN-28 cells, which exhibited the most resistance against apoptotic stimuli, expressed the highest level of caspase-9 beta. The induction of apoptosis by staurosporine or actinomycin D was markedly suppressed in caspase-9 beta-transfected HeLa cells. These results are consistent with our hypothesis that the caspase-9 beta may be an endogenous dominant-negative molecule which attenuates apoptotic activity in human gastric cancer cells. 相似文献
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Pichiorri F Ishii H Okumura H Trapasso F Wang Y Huebner K 《Journal of cellular biochemistry》2008,104(5):1525-1533
Common chromosome fragile sites occur at specific sequences within mammalian genomes that exhibit apparent single-stranded regions in mitotic chromosomes on exposure of cells to replication stress. Recent progress in the characterization of sequences, and more precise mapping of common fragile sites in mammalian and yeast genomes, has led to the exact placement of large common fragile regions straddling the borders of chromosomal G and R bands, with early and late replicating genomic regions, respectively, and could lead to breakthroughs in understanding the function of these evolutionarily conserved but highly recombinogenic chromosome elements. Deficiency of genes involved in DNA damage checkpoint responses, such as ATR, CHK1, HUS1 leads to increased frequency of fragile site instability. Some of these fragile sites, particularly FRA3B, encode genes that are themselves involved in the protection of cells from DNA damage through various mechanisms. Protection of mammalian genomes from accumulation of DNA damage in somatic cells is critical during development, puberty and during the reproductive lifespan, and occurs through mechanisms involving surveillance of the genome for damage, signals to the cell cycle machinery to stop cell cycle progression, signals to repair machinery to repair damage, signals to resume cycling or initiate apoptotic programs, depending on the extent of damage and repair. When genes involved in these processes are altered or deleted, cancer can occur. The tumor suppressor gene, FHIT at the FRA3B locus, and possibly other fragile genes, is a common target of damage and paradoxically encodes a protein with roles in protection from DNA damage. 相似文献
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