Premium
Alternative splicing of DNA polymerase β mRNA is not tumor‐specific
Author(s) -
Nowak Radoslawa,
Bieganowski Pawel,
Konopiński Ryszard,
Siedlecki Janusz A.
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19961009)68:2<199::aid-ijc10>3.0.co;2-6
Subject(s) - exon , alternative splicing , biology , microbiology and biotechnology , rna splicing , precursor mrna , messenger rna , dna polymerase , carcinogenesis , genomic dna , polymerase , splice , dna , genetics , gene , rna
Mammalian DNA polymerase β is a crucial enzyme in cell genomic maintenance. Its structure is highly conserved. Some splice variants of β‐pol mRNA were observed. One alternative splice DNA polymerase β mRNA, generated by 87 nt deletion (exon II) 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‐II‐deleted β‐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‐II alternative splicing variant of β‐pol mRNA is not tumor‐specific. © 1996 Wiley‐Liss, Inc.