作者: L. James , R. N. Eisenman
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摘要: The opposing transcriptional activities of the basic-helix-loop-helix-leucine zipper proteins Myc and Mad, taken together with information related to their expression patterns biological effects, have led a model Myc/Max/Mad network in which Mad function as antagonists. This antagonism is presumed operate at level genes targeted by these complexes, where Myc:Max activates Mad:Max represses same set genes. However, detailed analysis DNA-binding preferences for has not been performed. Furthermore, does address findings that indirectly transcription several regulatory To examine issues relating specificity responses, we determined Mad1 using selection amplification randomized oligonucleotides demonstrated its intrinsic identical c-Myc. We also used chimeric protein, containing substitution entire motif, shown it can reproduce growth-promoting Myc, but apoptotic function. Our results suggest although possessing vitro specificities, do an target vivo, apoptosis one outcome effects are directly antagonized those Mad.