Nowak R, Bieganowski P, Konopiński R, Siedlecki J A
Department of Molecular Biology, The Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland.
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.
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.
哺乳动物DNA聚合酶β是细胞基因组维持中的一种关键酶。其结构高度保守。已观察到β-pol mRNA的一些剪接变体。一种由该酶催化结构域中87个核苷酸缺失（外显子11）产生的选择性剪接DNA聚合酶β mRNA，被认为与肿瘤发生和遗传疾病（沃纳综合征）中的基因组不稳定有关。在此，我们表明，外显子11缺失的β-pol mRNA存在于所有检测的正常组织和肿瘤组织中，以及静息或PHA刺激的外周血单个核细胞中。这一发现证明，β-pol mRNA外显子11选择性剪接变体的存在并非肿瘤特异性的。
