Abstract
The deregulation of the human c-myc oncogene is associated with a variety of molecular defects, including translocations, gene amplification, and point mutations (Cole 1986). The relative contributions of these genetic alterations to the pathogenesis and progression of malignancy remain to be determined. Identification of genetic defects at the DNA sequence level helps to define the cis-elements which physiologically regulate c-myc expression. Conversely, elucidation of the components that normally control c-myc may provide insight into the pathogenetic mechanisms disrupting c-myc regulation. We have used a sensitive exonuclease protection assay to study the interaction of sequence-specific DNA binding proteins with potential regulatory sequences from the normal c-myc gene and from the abnormal c-myc allele derived from Burkitt’s lymphoma cells.KeywordsBurkitt LymphomaProtein Binding SitePutative Regulatory RegionRestriction Enzyme Cleavage SiteBurkitt Lymphoma Cell LineThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have