Alternative splicing of DNA polymerase beta mRNA is not tumor-specific

Int J Cancer. 1996 Oct 9;68(2):199-202. doi: 10.1002/(SICI)1097-0215(19961009)68:2<199::AID-IJC10>3.0.CO;2-6.

Abstract

Mammalian DNA polymerase beta is a crucial enzyme in cell genomic maintenance. Its structure is highly conserved. Some splice variants of beta-pol mRNA were observed. One alternative splice DNA polymerase beta mRNA, generated by 87 nt deletion (exon 11) in the catalytic domain of this enzyme, was suggested to be responsible for genomic instability in tumorigenesis and in genetic disorder (Werner syndrome). Here, we show that exon-11-deleted beta-pol mRNA is present in all examined normal and tumor tissues as well as in resting or PHA-stimulated peripheral-blood mononuclear cells. This finding proves that the presence of the exon-11 alternative splicing variant of beta-pol mRNA is not tumor-specific.

MeSH terms

  • Alternative Splicing*
  • Artifacts
  • DNA Polymerase I / genetics*
  • Exons / genetics*
  • Humans
  • Isoenzymes / genetics*
  • Male
  • Polymerase Chain Reaction
  • RNA, Messenger / genetics*
  • Testicular Neoplasms / genetics
  • Transcription, Genetic

Substances

  • Isoenzymes
  • RNA, Messenger
  • DNA Polymerase I