Reisman Lab Publications

Reisman, D., Balint, E., Loging, W.T., Rotter, V., and Almon, E., 1996 A novel transcript encoded within the 10-kb first intron of the human p53 tumor suppressor gene (D17S2179E) is induced during the differentiation of myeloid leukemia cells Genomics 39, 1648-1653.

Two promoters were previously shown to map to the 5'-end of the human p53 gene. p53p1 was located upstream of the first exon and is responsible for transcription of the major p53 mRNA species. p53p2 is a stronger promoter than p53p1 and was located within the 10,738-bp first intron, approximately 1000bp downstream of exon one. mRNA transcripts that initiated from p53p2 were previously identified in HL-60 cells by primer extension analysis and were observed to increase in abundance during differentiation of HL-60 cells to granulocytes. By screening a cDNA library with a probe derived from sequences downstream of the p53p2 start site, we have cloned and characterized a cDNA that represents a mRNA that appears to have been initiated from the p53p2 promoter. We have designated the gene encoding this transcript, Hp53int1 (the GDB designation is D17S2179E). The cDNA is 1125bp in length and is polyadenylated downstream from a consensus poly-A addition site. The entire 1125bp is derived from intron one of the p53 gene with no introns having been removed. The cDNA contains no major open reading frame although reading frame +1 contains a relatively low abundance of stop codons when compared to the other two reading frames and could possibly encode a protein of 119 amino acids. Analysis of the +1 reading frame shows a region of high homology to a portion of the DNA-binding domain of NFkB. These results indicate that a novel polyadenylated transcript is encoded by the first intron of the human p53 gene. Hp53int1 may be a pseudogene for a gene that may have encoded a DNA binding protein. Alternatively, the transcript may have a function since RNA transcripts of this gene are present in a number of human cells and their levels are induced during terminal differentiation of myeloid leukemia cells such as HL-60 and U937.