ArticleJournal of radiation research2015
Abundance of BER-related proteins depends on cell proliferation status and the presence of DNA polymerase β.
Article in Journal of radiation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- DNA polymerase β deficiency promotes the occurrence of esophageal precancerous lesions in mice.Neoplasia (New York, N.Y.) · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mammalian cells, murine N-methylpurine DNA glycosylase (MPG) removes bases damaged spontaneously or by chemical agents through the process called base excision repair (BER). In this study, we investigated the influence of POL β deficiency on MPG-initiated BER efficiency and the expression levels of BER-related proteins in log-phase and growth-arrested (G(0)) mouse embryonic fibroblasts (MEFs). G(0) wild-type (WT) or POL β-deficient (Pol β-KO) cells showed greater resistance to methyl methanesulfonate than did log-phase cells, and repair of methylated bases was less efficient in the G(0) cells. Apex1 mRNA expression was significantly lower in Pol β-KO or G(0) WT MEFs than in log-phase WT MEFs. Moreover, although Mpg mRNA levels did not differ significantly among cell types, MPG protein levels were significantly higher in log-phase WT cells than in log-phase Pol β-KO cells or either type of G(0) cells. Additionally, proliferating cell nuclear antigen protein levels were also reduced in log-phase Pol β-KO cells or either type of G(0) cells. These results indicated that MPG-initiated BER functions mainly in proliferating cells, but less so in G(0) cells, and that POL β may be involved in regulation of the amount of intracellular repair proteins.
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Registered trials
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