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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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s-Myc acts as a transcriptional activator and its sequence-specific DNA binding is required for induction of programmed cell death in glioma cells.

We previously reported that s-Myc expression effectively induces programmed cell death (PCD) by apoptosis in glioma cells that express only mutated p53. To determine the molecular mechanism of s-Myc-induced PCD, we examined the correlation between transcriptional activation of s-Myc and its ability to induce PCD. Using a reporter plasmid having an upstream promoter region containing four repeats of the hexanucleotide CACGTG, we found that s-Myc can activate transcription of a reporter gene from this plasmid. Two mutated forms of s-Myc protein, s-MycCKII and s-MycmBR, were created. While s-MycCKII whose casein kinase (CK) II cognate sequence was restored in the internal acidic domain activated transcription as efficiently as wild-type s-Myc and induced PCD in glioma cells, s-MycmBR having a mutated basic region unable to bind the CACGTG motif did not. These findings suggest that transactivation activity of s-Myc through sequence-specific DNA binding may be indispensable for induction of PCD but that lack of a CK-II cognate sequence in the internal acidic domain may have little effect on these functions of s-Myc.[1]

References

  1. s-Myc acts as a transcriptional activator and its sequence-specific DNA binding is required for induction of programmed cell death in glioma cells. Kitanaka, C., Sugiyama, A., Kanazu, S., Miyagi, Y., Mishima, K., Asai, A., Kuchino, Y. Cell Death Differ. (1995) [Pubmed]
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