Profile Details

Research Interest

Molecular architecture of growth regulatory signal transduction cascades
Cancer
Signal transduction
Oncogenes
Tumor Suppressors

Faculty Research Bio

The broad goal of our research is to contribute to uncovering the molecular nature of cell autonomous regulatory mechanisms permitting appropriate responses of human cells to their environment. These mechanisms are ultimately responsible for initiating correct developmental and adaptive changes in cell behavior. Aberrant regulation of these mechanisms results in pathological changes that are responsible for initiating a wide variety of human diseases including cancer. Our focus has been on the contribution of Ras-family small GTPases to the regulation of proliferation, differentiation, and oncogenic transformation. Our work has shown that these proteins act as key nodes in signal transduction networks, integrating extracellular and intracellular cues to the activation of appropriate machinery driving the response of cells to those cues. We are defining the composition, organization, and regulation of the Ras GTPase signaling network. We are using this information to establish paradigms describing the nature of signal-mediated information flow and connectivity to cell biological responses. With respect to human disease, we are translating our observations into a molecular understanding of the establishment of a minimal tumorigenic platform in general, and into defining the critical contribution of Ras oncogenes to initiation and maintenance of human cancer in particular.

Address

UT Southwestern Medical Center at Dallas
5323 Harry Hines Blvd
Dallas, Texas 75390

Contact:

214-648-2861

Recent Publications

Matheny, S., Chen, C., Kortum, R., Razidlo, G., Lewis, R., and White, M. A. , " Ras regulates assembly of mitogenic signaling complexes through the novel effector protein IMP. "Nature ,427:256-260 ,2004

Chien Y, Kim S, Bumeister R, Loo YM, Kwon SW, Johnson CL, Balakireva MG, Romeo Y, Kopelovich L, Gale M Jr, Yeaman C, Camonis JH, Zhao Y, White MA , " RalB GTPase-mediated activation of the IkappaB family kinase TBK1 couples innate immune signaling to tumor cell survival "Cell ,6:157-170 ,October 2006

Whitehurst, A. W., Bodemann, B. O., Cardenas, J., Ferguson, D., Girard, L., Payton, M., Minna, J. D., Michnoff, C., Hao, W., Roth, M. G., Xie X.-J., and White, M. A. , " Functional genomics of chemosensitivity exposes deviant cancer cell regulatory systems. "Nature ,446:815-820 ,2007

Bodemann BO, Orvedahl A, Cheng T, Ram RR, Ou YH, Formstecher E, Maiti M, Hazelett CC, Wauson EM, Balakireva M, Camonis JH, Yeaman C, Levine B, White MA. , " RalB and the exocyst mediate the cellular starvation response by direct activation of autophagosome assembly. "Cell ,144:253-267 ,January 2011

OU YH, Torres M, Ram R, Formstecher E, Roland C, Cheng T, Brekken R, Wurz R, Tasker A, Polverino T, Tan SL, White MA. , " TBK1 Directly Engages Akt/PKB Survival Signaling to Support Oncogenic Transformation. "Molecular Cell ,41/4:458-470 ,February 2011