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pubmed:abstractText |
The oncogenic activity of c-MYC is well known, and genetic aberrations in this locus are associated with a variety of human neoplasms. Because the encoded MYC protein has transcriptional activity only when dimerized with MAX, it is possible that mutations of MAX also could have phenotypic consequences. We have now found, by fluorescence in situ hybridization and quantified Southern blot analyses, that the MAX gene has been reduced to hemizygosity in HL60 cells. Although the sequence of the coding region of the remaining allele of the MAX gene is not mutated, this reduction in gene dosage may be the cause of a lower abundance of MAX protein in these cells that could result in an imbalance in the complex transcription factor network in which MAX has a pivotal role.
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