title: Transcriptional arrest within the first exon is a fast control mechanism in c-myc gene expression.
abstract: DMSO (dimethylsulfoxide), a potent inducer of granulocytic differentiation in HL60 cells, causes a rapid decrease of cytoplasmic steady state c-myc RNA. This decrease is regulated mainly at the level of transcript elongation. Elongation is blocked within the untranslated c-myc leader. Twelve hours after transcriptional shut off of c-myc, DNAase I hypersensitive site II was still detectable, indicating that closing of this site upstream of the gene does not correlate with reduction in the steady state level of c-myc RNA.
mesh_terms: D001483:Base Sequence; D002454:Cell Differentiation; D002460:Cell Line; D004121:Dimethyl Sulfoxide / Q000494:pharmacology*; D005091:Exons; D005796:Genes; D005809:Genes, Regulator; D006801:Humans; D007438:Introns; D015470:Leukemia, Myeloid, Acute; D009690:Nucleic Acid Conformation; D009693:Nucleic Acid Hybridization; D009857:Oncogenes; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D016271:Proto-Oncogene Proteins c-myc; D012334:RNA, Neoplasm / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects*
chemical_list: D011518:Proto-Oncogene Proteins; D016271:Proto-Oncogene Proteins c-myc; D012334:RNA, Neoplasm; D004121:Dimethyl Sulfoxide