Telomere dysfunction impairs DNA repair and enhances sensitivity to ionizing radiation
β Scribed by DePinho, Ronald A.; Wong, Kwok-Kin; Chang, Sandy; Weiler, Sarah R.; Ganesan, Shridar; Chaudhuri, Jayanta; Zhu, Chengming; Artandi, Steven E.; Rudolph, Karl Lenhard; Gottlieb, Geoffrey J.; Chin, Lynda; Alt, Frederick W.
- Book ID
- 109828892
- Publisher
- Nature Publishing Group
- Year
- 2000
- Tongue
- English
- Weight
- 722 KB
- Volume
- 26
- Category
- Article
- ISSN
- 1061-4036
- DOI
- 10.1038/79232
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
## Abstract About 45% of head and neck squamous cell carcinomas (HNSCC) are characterized by amplification of chromosomal band 11q13. This amplification occurs by a breakageβfusionβbridge (BFB) cycle mechanism. The first step in the BFB cycle involves breakage and loss of distal 11q, from __FRA11F_
## Abstract In doubleβstrand DNA damage repair, nonhomologous end joining (NHEJ) is more errorβprone than homologous recombination repair (HRR), indicating that the relative prevalence of NHEJ may lead to more incorrect repair and thus to increases in chromosome damage. If DNA damage is extensive a
ATM and DNA-dependent protein kinase catalytic subunit (DNA-PKcs) have been shown to have sequences homologous to the catalytic domains of mammalian phosphatidylinositol 3-kinase (PI3-kinase). In order to determine the contribution of ATM and DNA-PKcs to the increased sensitivity of cells to DNA-dam