Access

You are not currently logged in.

Access your personal account or get JSTOR access through your library or other institution:

login

Log in to your personal account or through your institution.

If You Use a Screen Reader

This content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.

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
Radiation Research
Vol. 156, No. 5, Part 1 (Nov., 2001), pp. 535-544
Stable URL: http://www.jstor.org/stable/3580576
Page Count: 10
  • Read Online (Free)
  • Download ($10.00)
  • Subscribe ($19.50)
  • Cite this Item
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
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
Preview not available

Abstract

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.

Page Thumbnails

  • Thumbnail: Page 
535
    535
  • Thumbnail: Page 
536
    536
  • Thumbnail: Page 
537
    537
  • Thumbnail: Page 
538
    538
  • Thumbnail: Page 
539
    539
  • Thumbnail: Page 
540
    540
  • Thumbnail: Page 
541
    541
  • Thumbnail: Page 
542
    542
  • Thumbnail: Page 
543
    543
  • Thumbnail: Page 
544
    544