A tale of three PKCs
نویسنده
چکیده
374 Cell Cycle Volume 10 Issue 3 The proto-oncogene MYC encodes an essential master-regulatory protein in normal cells that controls a variety of critical cellular processes, including proliferation, apoptosis and differentiation.1 When the tightly regulated expression of Myc in normal cells becomes deregulated, Myc becomes a potent oncogene that can drive tumor initiation and progression. Myc deregulation plays a profound role in tumorigenesis and is thought to contribute to the development of over 50% of human cancers of diverse origin. Defining the molecular mechanisms underlying both proto-oncogenic and oncogenic Myc function promises to yield important advances in the development of useful anticancer therapeutics targeting Myc activity. Past research efforts largely focused on understanding how Myc functions as a regulator of gene transcription, with the identification of target genes taking center stage. Current advances have demonstrated that Myc binds to the promoter regions of many gene targets, yet only a subset are then regulated at the level of expression. Moreover, to add further complexity, Myc has recently been reported in the cytoplasm.2 The role Myc plays in this new subcellular compartment remains unclear. Although evidence suggests that recruitment of co-regulators is essential for Myc function,3 further insight into the specific molecular mechanisms controlling Myc-dependent transformation are required. An important yet understudied strategy to delineate Myc’s mechanisms of action is to identify Myc partner proteins, and then to subsequently equate these protein complexes to their functional roles and biological activities. A handful of Myc-binding proteins have been identified to date, with the best-studied example being Max.4,5 The Myc:Max interaction appears to be essential for Myc activation and repression of gene transcription, as well as for most Myc-related biological activities. Despite Cell Cycle News & Views
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