| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8232301 | International Journal of Radiation Oncology*Biology*Physics | 2010 | 8 Pages |
Abstract
Both RalA and RalB contribute to K-Ras-dependent IR resistance of MIA PaCa-2 cells. Sensitization due to suppressed Ral expression is likely due in part to decreased efficiency of DNA repair (RalA and RalB) and increased susceptibility to apoptosis (RalB). Ral-mediated radioresistance does not depend on either the RalBP1 or the exocyst complex, the two best-characterized Ral effectors, and instead may utilize an atypical or novel effector.
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Authors
Ambrose R. Ph.D., Jared L. Ph.D., Timothy D. B.S., Sarah F. M.D., Channing J. Ph.D., Adrienne D. Ph.D.,