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Identification of KIN (KIN17), a Human Gene Encoding a Nuclear DNA-Binding Protein, as a Novel Component of the TP53-Independent Response to Ionizing Radiation
Christel Masson, Farid Menaa, Ghislaine Pinon-Lataillade, Yveline Frobert, J. Pablo Radicella and Jaime F. Angulo
Vol. 156, No. 5, Part 1 (Nov., 2001), pp. 535-544
Published by: Radiation Research Society
Stable URL: http://www.jstor.org/stable/3580576
Page Count: 10
You can always find the topics here!Topics: RNA, Cell lines, Irradiation, Ionizing radiation, Up regulation, Genes, DNA, Tumors, DNA damage, Gels
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Ionizing radiation elicits a genetic response in human cells that allows cell survival. The human KIN (also known as KIN17) gene encodes a 45-kDa nuclear DNA-binding protein that participates in the response to UVC radiation and is immunologically related to the bacterial RecA protein. We report for the first time that ionizing radiation and bleomycin, a radiomimetic drug, which produce single- and double-strand breaks, increased expression of KIN in human cells established from tumors, including MeWo melanoma, MCF7 breast adenocarcinoma, and ATM(+)GM3657 lymphoblast cells. KIN expression increased rapidly in a dose-dependent manner after irradiation. Under the same conditions, several genes controlled by TP53 were induced with kinetics similar to that of KIN. Using the CDKN1A gene as a marker of TP53 responsiveness, we analyzed the up-regulation of KIN and showed that is independent of the status of TP53 and ATM. In contrast, the presence of a dominant mutant for activating transcription factor 2 (ATF2) completely abolished the upregulation of KIN. Our results suggest a role for ATF2 in the TP53-independent increase in KIN expression after γ irradiation.
Radiation Research © 2001 Radiation Research Society