Email RIS file
Bookmark
Report an Issue

Nuclear apoJ [electronic resource] : An X-ray-inducible cell death signal. Final Report

Published
Washington, D.C. : United States. Dept. of Energy. Office of Energy Research, 2003.
Oak Ridge, Tenn. : Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy
Physical Description
vp : digital, PDF file
Additional Creators
United States. Department of Energy. Office of Energy Research and United States. Department of Energy. Office of Scientific and Technical Information
Access Online

Availability

I Want It
I Want It

Finding items...

Restrictions on Access
Free-to-read Unrestricted online access
Summary
The complex interactions between apoptosis, genomic instability and carcinogenesis induced by low dose ionizing radiation (IR) are poorly understood. Tissues differentially withstand IR based on complex processes that include DNA repair, altered gene expression, and apoptosis. This proposal is based on the investigators' discovery of a protein, apoJ (initially designated xip8/XIP8), that is dramatically IR-induced. The protein is also known as a marker for apoptosis, but its function is unknown. The ''nuclear'' form of the apoJ protein, undergoes dramatic accumulation in the nucleus following IR, and then strongly associates with the C-terminus of Ku70, a key factor in DNA-PK-dependent nonhomologous DNA double strand break (DSB) repair. These studies suggest that the nuclear form of apoJ is a major determinant in the elimination of carcinogenic cells and that it contributes strongly to nonlinearity threshold responses for survival and carcinogenesis.
Report Numbers
E 1.99:doe/er/--62724-1
doe/er/--62724-1
Subject(s)
Note
Published through SciTech Connect.
12/29/2003.
"doe/er/--62724-1"
David A. Boothman.
Case Western Reserve Univ., Cleveland, OH (United States)
Type of Report and Period Covered Note
Final; 10/30/1998 - 10/31/2001
Funding Information
FG02-99ER62724
View MARC record | catkey: 23501430