DNA polymerase activity in a repair-deficient human cell line |
| |
| Authors: | C O Joe J O Norman T R Irvin D L Busbee |
| |
| Affiliation: | 1. Department of Anatomy, College of Veterinary Medicine, Texas A & M University, College Station, TX 77843 USA;2. Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A & M University, College Station, TX 77843 USA;3. Veterinary Toxicology and Entomology Research Laboratory, ARS, USDA, College Station, TX 77841 USA;1. Genome Center, University of California, Davis, 451 Health Sciences Drive, Davis, CA 95616, United States;2. Graduate Group of Applied Mathematics, University of California, Davis, 1, Shields Ave, Davis, CA, 95616, United States;3. Department of Computer Science and Genome Center, University of California, Davis, 1, Shields Ave, Davis, CA, 95616, United States;1. Fakultät Statistik, Technische Universität Dortmund, 44221 Dortmund, Germany;2. Institute for Complex Systems and Mathematical Biology, University of Aberdeen, Aberdeen AB24 3UE, United Kingdom;1. University of Murcia, Murcia, Spain;2. Catholic University of Murcia, Murcia, Spain |
| |
| Abstract: | A human low-density-lipoprotein (LDL) receptor-deficient diploid fibroblast cell line (GM1915) was determined to be short patch competent (DNA polymerase-beta) and long patch deficient (DNA polymerase-alpha) for DNA excision repair. Analysis of DNA from GM1915 cells or from WI38 control cells, following treatment with a mutagen known to initiate long patch excision repair, showed that GM1915 cells exhibited decreased resynthesis of oligonucleotide segments excised during repair. When cells deficient in DNA polymerase-alpha activity were permeabilized to permit LDL entry, repair synthesis immediately increased. These data suggest that DNA polymerase-alpha is not activated by mutagen treatment in GM1915 cells and that introduction of LDL into the cells results in activation of the enzyme. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
