|
|
Dr. Steven L. Sanders
Assistant Professor
- Biochemistry Trainer: YES
- Phone: 216 235 1858
- Fax: 216 368 3419
- Office: RT400-8
- Lab: RT400
- Sanders Lab Page
- Mail Address:
Department of Biochemistry
10900 Euclid Avenue
Cleveland, OH 44106-4935
Dr. Steven L. Sanders
The goal of my research is to understand how chromatin is regulated during processes that govern genome stability and how deregulation of chromatin function contributes to the development of cancer. More specifically the laboratory is focused on elucidating how enzymes that mark histones by post-translational modification function in DNA damage response.
To insure their genetic integrity cells employ a multitude of DNA damage response pathways. The importance of these pathways is illustrated by the fact that deregulation is linked to a number of cancer prone diseases. A myriad of DNA damage response factors have been characterized, but how these factors contend with the highly compact and generally inhibitory state of chromatin, the native genetic template, is an open question. Chromatin-modifying activities, such as post-translational modification of histones, are utilized by the cell's transcriptional machinery to contend with chromatin. How these modifying activities might also contribute to DNA damage response is poorly understood. Addressing this deficiency is of vital importance as mounting evidence argues deregulation of chromatin-modifying enzymes may play a central role during oncogenesis. The goal of the laboratory is to decipher how histone-modifying enzymes function during DNA damage response. We are particularly interested in those factors that have been conserved throughout eukaryotic evolution from yeast to man. This allows us to utilize the genetic and biochemical power of model yeast organisms to rapidly dissect regulatory pathways that have implications for human disease.
Selected References
- Sanders, S. L., Portoso, M., Mata, J., Bahler, J., Allshire, R. C., Kouzarides, T. (2004). Methylation of histone H4 lysine 20 controls recruitment of Crb2 to sites of DNA damage. Cell 119, 603-614. Cell 2004 119:603-14
|
