ArticleNucleic acids research2011
Restoration of G1 chemo/radioresistance and double-strand-break repair proficiency by wild-type but not endonuclease-deficient Artemis.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Nucleases and Their Inhibitors: Exploring Biological Roles, Industrial Applications, and Challenges in Heterologous Expression.Biotechnology journal · 2026Review
- Modeling the interplay between DNA-PK, Artemis, and ATM in non-homologous end-joining repair in G1 phase of the cell cycle.Journal of biological physics · 2019Article
- Silencing Artemis Enhances Colorectal Cancer Cell Sensitivity to DNA-Damaging Agents.Oncology research · 2018Article
- TDP1 suppresses mis-joining of radiomimetic DNA double-strand breaks and cooperates with Artemis to promote optimal nonhomologous end joining.Nucleic acids research · 2018Article
- The Interaction of the Metallo-Glycopeptide Anti-Tumour Drug Bleomycin with DNA.International journal of molecular sciences · 2018Review
- Structure-Specific nuclease activities of Artemis and the Artemis: DNA-PKcs complex.Nucleic acids research · 2016Article
- Effects of hyperthermia on DNA repair pathways: one treatment to inhibit them all.Radiation oncology (London, England) · 2015Review
- PARP-2 depletion results in lower radiation cell survival but cell line-specific differences in poly(ADP-ribose) levels.Cellular and molecular life sciences : CMLS · 2015Article
- Involvement of p53 in the repair of DNA double strand breaks: multifaceted Roles of p53 in homologous recombination repair (HRR) and non-homologous end joining (NHEJ).Sub-cellular biochemistry · 2014Review
- Trimming of damaged 3' overhangs of DNA double-strand breaks by the Metnase and Artemis endonucleases.DNA repair · 2013Article
- Artemis is required to improve the accuracy of repair of double-strand breaks with 5'-blocked termini generated from non-DSB-clustered lesions.Mutagenesis · 2013Article
- Elevated expression of artemis in human fibroblast cells is associated with cellular radiosensitivity and increased apoptosis.British journal of cancer · 2012Article
- Processing of damaged DNA ends for double-strand break repair in mammalian cells.ISRN molecular biology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Deficiency in Artemis is associated with lack of V(D)J recombination, sensitivity to radiation and radiomimetic drugs, and failure to repair a subset of DNA double-strand breaks (DSBs). Artemis harbors an endonuclease activity that trims both 5'- and 3'-ends of DSBs. To examine whether endonucleolytic trimming of terminally blocked DSBs by Artemis is a biologically relevant function, Artemis-deficient fibroblasts were stably complemented with either wild-type Artemis or an endonuclease-deficient D165N mutant. Wild-type Artemis completely restored resistance to γ-rays, bleomycin and neocarzinostatin, and also restored DSB-repair proficiency in G0/G1 phase as measured by pulsed-field gel electrophoresis and repair focus resolution. In contrast, cells expressing the D165N mutant, even at very high levels, remained as chemo/radiosensitive and repair deficient as the parental cells, as evidenced by persistent γ-H2AX, 53BP1 and Mre11 foci that slowly increased in size and ultimately became juxtaposed with promyelocytic leukemia protein nuclear bodies. In normal fibroblasts, overexpression of wild-type Artemis increased radioresistance, while D165N overexpression conferred partial repair deficiency following high-dose radiation. Restoration of chemo/radioresistance by wild-type, but not D165N Artemis suggests that the lack of endonucleolytic trimming of DNA ends is the principal cause of sensitivity to double-strand cleaving agents in Artemis-deficient cells.
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Registered trials
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