Ruth W. Craig, Ph.D.
Professor of Pharmacology and Toxicology
Hanover, NH 03755
Phone: (603) 650-1657
Dr. Craig's research is centered on understanding the role of MCL1 and other members of the BCL2 family in normal cell development and in cancer. MCL1, BCL2, and pro-survival members of this family maintain cell viability, while other family members cause cell death. Expression of these gene products controls the survival of cells as they pass through successive stages of differentiation. Expression is modulated by environmental cues such as growth and differentiation factors. This serves to maintain and amplify cell types and lineages that are needed by the organism, while eliminating cells that are not needed or are damaged or senescent. However, loss of the normal regulated pattern of expression of MCL1 or other family members can allow for prolonged survival of cells that would normally die. This, in turn, allows for the acquisition of genetic changes that can initiate the development of cancer.
The work in Dr. Craig's laboratory focuses on how MCL1 and other pro-survival genes contribute to the ongoing maintenance of homeostasis in hematopoietic and lymphoid cells, and on how alterations affecting the regulation of these genes can lead to the development of leukemia and lymphoma. The long-term goal is to utilize understanding of the role of genes that control survival, prominently MCL1, in order to regulate normal B-, T-, and hematopoietic cell development and to inhibit tumorigenesis.
Nifoussi, S. K., Vrana, J. A., Domina, A. M., De Biasio, A., Gui, J., Gregory, M. A., Hann, S. R., and Craig, R. W. Thr 163 Phosphorylation Causes Mcl-1 Stabilization When Degradation is Independent of the Adjacent GSK3-targeted Phosphodegron, Promoting Drug Resistance in Cancer, Plos One, in press.
For a complete listing of publications on PubMed, click here.