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National Cancer Institute®
Last Modified: September 1, 2002
1
UI - 11420261
AU - Gottlieb S
TI -
Scientists screen embryo for genetic predisposition to cancer.
SO - BMJ 2001 Jun 23;322(7301):1505
2
UI - 7663514
AU - Wang XW; Yeh H; Schaeffer L; Roy R; Moncollin V; Egly JM; Wang Z;
TI -
Freidberg EC; Evans MK; Taffe BG; et al
p53 modulation of TFIIH-associated nucleotide excision repair activity.
SO - Nat Genet 1995 Jun;10(2):188-95
AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National
Institutes of Health, Bethesda, Maryland 20892-4255, USA.
p53 has pleiotropic functions including control of genomic plasticity
and integrity. Here we report that p53 can bind to several transcription
factor IIH-associated factors, including transcription-repair factors,
XPD (Rad3) and XPB, as well as CSB involved in strand-specific DNA
repair, via its C-terminal domain. We also found that wild-type, but not
Arg273His mutant p53 inhibits XPD (Rad3) and XPB DNA helicase
activities. Moreover, repair of UV-induced dimers is slower in
Li-Fraumeni syndrome cells (heterozygote p53 mutant) than in normal
human cells. Our findings indicate that p53 may play a direct role in
modulating nucleotide excision repair pathways.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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