| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Advances in Brief |
Howard Hughes Medical Institute [J. C., J. G.], Department of Molecular Genetics, Biochemistry, and Microbiology [G. L., J. C., J. G.], and Department of Environmental Health [J. E., Y. L., K. D.], The University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524
Experiments with the supF20 mutagenesis system demonstrate that extracts from Bloom’ssyndrome (BS) cells are unable to use microhomology elements within the supF20 gene to restore supF function after the induction of a double-strand break (DSB). Additional experiments with the pUC18 mutagenesis system demonstrate that although the efficiency and fidelity of DSB repair by BS extracts are comparable with those of normal extracts when ligatable ends are present, a significant 5-fold increase in mutation rate with BS extracts is observed when terminal phosphates are removed from the DNA substrate that needs repair. Mutant plasmids recovered after DSB repair by BS extracts contain smaller deletions within the lacZ
gene not commonly recovered from normal extracts. This work demonstrates that BS cells, lacking the BLM helicase, process DSBs differently than normal cells and strongly suggests a role for the BLM helicase in aligning microhomology elements during recombinational events in DSB repair.
This article has been cited by other articles:
|
|
 |
|
  C. Wilson, S. Idziaszczyk, J. Colley, V. Humphreys, C. Guy, J. Maynard, J. R. Sampson, and J. P. Cheadle Induction of Renal Tumorigenesis with Elevated Levels of Somatic Loss of Heterozygosity in Tsc1+/- Mice on a Blm-Deficient Background Cancer Res., November 15, 2005; 65(22): 10179 - 10182. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Paz-Elizur, D. E. Brenner, and Z. Livneh Interrogating DNA Repair in Cancer Risk Assessment Cancer Epidemiol. Biomarkers Prev., July 1, 2005; 14(7): 1585 - 1587. [Full Text] [PDF]
|
|
|
|
 |
|
 S. Jacob, C. Miquel, A. Sarasin, and F.ço. Praz Effects of camptothecin on double-strand break repair by non-homologous end-joining in DNA mismatch repair-deficient human colorectal cancer cell lines Nucleic Acids Res., January 7, 2005; 33(1): 106 - 113. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. So, N. Adachi, M. R. Lieber, and H. Koyama Genetic Interactions between BLM and DNA Ligase IV in Human Cells J. Biol. Chem., December 31, 2004; 279(53): 55433 - 55442. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sengupta, A. I. Robles, S. P. Linke, N. I. Sinogeeva, R. Zhang, R. Pedeux, I. M. Ward, A. Celeste, A. Nussenzweig, J. Chen, et al. Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrest J. Cell Biol., September 13, 2004; 166(6): 801 - 813. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. Braybrooke, J.-L. Li, L. Wu, F. Caple, F. E. Benson, and I. D. Hickson Functional Interaction between the Bloom's Syndrome Helicase and the RAD51 Paralog, RAD51L3 (RAD51D) J. Biol. Chem., November 28, 2003; 278(48): 48357 - 48366. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Onclercq-Delic, P. Calsou, C. Delteil, B. Salles, D. Papadopoulo, and M. Amor-Gueret Possible anti-recombinogenic role of Bloom's syndrome helicase in double-strand break processing Nucleic Acids Res., November 1, 2003; 31(21): 6272 - 6282. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. H. Goss, M. A. Risinger, J. J. Kordich, M. M. Sanz, J. E. Straughen, L. E. Slovek, A. J. Capobianco, J. German, G. P. Boivin, and J. Groden Enhanced Tumor Formation in Mice Heterozygous for Blm Mutation Science, September 20, 2002; 297(5589): 2051 - 2053. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
