David A Fruman
Molecular Biology & Biochemistry
School of Biological Sciences
Phone: (949) 824-1947
Email: dfruman@uci.edu
mbb.bio.uci.edu/fruman/
http://www.faculty.uci.edu/profile.cfm?faculty_id=4541
David Fruman
The focus of research in Dr. Fruman’s laboratory is signal transduction in lymphocytes. The long-term goal is to define signaling components whose function is specific to particular immune cell types or responses. Their rationale is that such components could prove useful as therapeutic targets for immunological diseases and cancer. Phosphoinositide 3-kinase (PI3K) is one signaling molecule that has well-established roles in control of growth and survival of both normal and cancer cells. The PI3K pathway is complex, with many potential downstream effectors and several isoforms of PI3K itself. Work in Dr. Fruman’s laboratory is divided into three general areas: (1) Specificity of PI3K signaling in immune cells; (2) Role of the PI3K pathway in leukemic transformation; (3) Transcription factors that oppose lymphocyte proliferation and leukemia.
Selected Publications:
Kharas, M. G., Deane, J. A., Wong, S., O'Bosky, K. R., Rosenberg, N., Witte, O. N., and Fruman, D. A. (2004). Phosphoinositide 3-kinase signaling is essential for ABL oncogene-mediated transformation of B-lineage cells. Blood 103(11), 4268-75.
Kharas, M. G., and Fruman, D. A. (2005). ABL oncogenes and phosphoinositide 3-kinase: mechanism of activation and downstream effectors. Cancer Res 65(6), 2047-53.
Oak, J. S., Deane, J. A., Kharas, M. G., Luo, J., Lane, T. E., Cantley, L. C., and Fruman, D. A. (2006). Sjogren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase. Proc Natl Acad Sci U S A 103(45), 16882-7.
Deane, J. A., Kharas, M. G., Oak, J. S., Stiles, L. N., Luo, J., Moore, T. I., Ji, H., Rommel, C., Cantley, L. C., Lane, T. E., and Fruman, D. A. (2007). T-cell function is partially maintained in the absence of class IA phosphoinositide 3-kinase signaling. Blood 109(7), 2894-902.
Kharas, M. G., Yusuf, I., Scarfone, V. M., Yang, V. W., Segre, J. A., Huettner, C. S., and Fruman, D. A. (2007). KLF4 suppresses transformation of pre-B cells by ABL oncogenes. Blood 109(2), 747-55. |
