Research in our laboratory focuses on the maintenance of chromosome stability by homologous recombination (HR) DNA repair mechanisms. Accumulation of chromosome rearrangements is often observed during cancer progression, and using the laboratory mouse as a model system, we are studying mutations in HR genes.
- DNA Repair
- Chromosome Instability
- Mouse Genetics
- Homologous Recombination
- Cancer Research
- Rajesh, C. and Pittman, D.L. (2006) Cell Cycle Regulation in Mammalian Germ Cells. In: Kaldis, P. (ed.) Cell Cycle Regulation. Results and Problems in Cell Differentiation, vol. 42. Springer Berlin, Heidelberg, New York, pp 343-368.
- Smiraldo PG, Gruver AM, Osborn JC, Pittman DL. Extensive chromosomal instability in Rad51d-deficient mouse cells. Cancer Res. 2005 Mar 15;65(6):2089-2096.
- Gruver AM, Miller KA, Rajesh C, Smiraldo PG, Kaliyaperumal S, Balder R, Stiles KM, Albala JS, Pittman DL. The ATPase motif in RAD51D is required for resistance to DNA interstrand crosslinking agents and interaction with RAD51C. Mutagenesis. 2005 Nov;20(6):433-440.
- Tarsounas M., Munoz, P., Claas A., Smiraldo P.G., Pittman D.L., Blasco, M.A. and S.C. West. (2004) Telomere Maintenance Requires the RAD51D Recombination/Repair Protein. Cell 117(3):337-347,