Titlebook: Ataxia-Telangiectasia; Richard A. Gatti,Robert B. Painter Conference proceedings 1993 Springer-Verlag Berlin Heidelberg 1993 Ataxia-Telang

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書目名稱Ataxia-Telangiectasia影響因子(影響力)




書目名稱Ataxia-Telangiectasia影響因子(影響力)學(xué)科排名




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書目名稱Ataxia-Telangiectasia網(wǎng)絡(luò)公開度學(xué)科排名




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信條

Frankreichs Verfassung 1958–2008ations were the cause for the increased incidence and suggested, therefore, that mammography screening may not be beneficial for A-T heterozygotes. We emphatically disagree: mammography screening is particularly beneficial for A-T heterozygotes whose risk for breast cancer is higher than for the general population.

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Conference proceedings 1993e body parts ascerebellum, thymus and chromosomes. The patients areundulysensitive to ionizing radiation, immunodeficient, and athird of them develops cancer. All of this stems fromdefects of a singlegene.Provided here is an up-to-date review of all important workin thefield. A wide spectrum of topi

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擁護(hù)

Bildungsdiskussionen in Frankreichd A,C,D and E) have been described (Jaspers ., 1988); although the disease is clinically indistinguishable in the four groups, radiation-sensitivity is rendered normal by fusion of cells deriving from A-T patients from different groups (whereas fusion of cells from patients from the same group has no effect).

defenses

https://doi.org/10.1007/978-3-531-91665-1 to a defect in rejoining of radiation-induced DNA double strand breaks. Hence, the site-specific V(D)J DNA recombination process has been linked to the repair of randomly-induced double-strand breaks.

GRE

Cloning and Characterization of a Candidate Gene for A-T Complementation Group Dtially radioresistant when compared with the original A-T cell line. This approach was begun in this Laboratory in 1983 and resulted in the isolation of a candidate A-T gene at the end of 1990. Currently, work is in progress to characterize this candidate gene and to determine whether it is the gene for A-T complementation group D.

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LINES

Murine scid cells and human ataxia-telangiectasia cells complement each other’s radiosensitivity to a defect in rejoining of radiation-induced DNA double strand breaks. Hence, the site-specific V(D)J DNA recombination process has been linked to the repair of randomly-induced double-strand breaks.