作者: Emily J. Chenette , Gretchen A. Repasky , Channing J. Der
关键词:
摘要: Ras proteins activate cytoplasmic signaling cascades that mediate responses in growth, cellular differentiation, and survival. Therefore, it is not surprising mutationally activated have been found many human cancers. Determining the effector protein pathways through which causes transformation important for creating targeted therapeutics will specifically block oncogenic effects of Ras. In 1993, Raf serine/threonine kinases were identified as key downstream effectors transformation. While remains best characterized effector, rapid expansion pool has demonstrated transforming activity also mediated by Raf-independent pathways. These include phosphatidylinositol 3-kinase phospholipase regulators phospholipid metabolism, guanine nucleotide exchange factors activators Ras-related proteins. Further complexity arose when a new seemingly incongruous group pro-apoptotic with tumor suppressor function was identified. This chapter summarize recent findings mutational activation B-Raf cancers examine importance non-Raf Ras-mediated