ArticleCell death & disease2016
Overexpression of the scaffold WD40 protein WRAP53β enhances the repair of and cell survival from DNA double-strand breaks.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Low levels of WRAP53 predict decreased efficacy of radiotherapy and are prognostic for local recurrence and death from breast cancer: a long-term follow-up of the SweBCG91RT randomized trial.Molecular oncology · 2023Trial
- WRAP53 is Downregulated in Acute Myeloid Leukemia Patients and Positively Correlates With HTERT Expression.Cancer reports (Hoboken, N.J.) · 2026Article
- RNA binding proteins (RBPs) and their role in DNA damage and radiation response in cancer.Advanced drug delivery reviews · 2022Review
- The Role of WRAP53 in Cell Homeostasis and Carcinogenesis Onset.Current issues in molecular biology · 2022Review
- Small Cajal body-associated RNA 2 (scaRNA2) regulates DNA repair pathway choice by inhibiting DNA-PK.Nature communications · 2022Article
- Genome-Wide Association Study for Ultraviolet-B Resistance in Soybean (Plants (Basel, Switzerland) · 2021Article
- Non-canonical roles of canonical telomere binding proteins in cancers.Cellular and molecular life sciences : CMLS · 2021Review
- Suppression of TCAB1 expression induced cellular senescence by lessening proteasomal degradation of p21 in cancer cells.Cancer cell international · 2021Article
- New Faces of old Friends: Emerging new Roles of RNA-Binding Proteins in the DNA Double-Strand Break Response.Frontiers in molecular biosciences · 2021Review
- Biallelic mutations in WRAP53 result in dysfunctional telomeres, Cajal bodies and DNA repair, thereby causing Hoyeraal-Hreidarsson syndrome.Cell death & disease · 2020Article
- The Cajal Body Protein WRAP53β Prepares the Scene for Repair of DNA Double-Strand Breaks by Regulating Local Ubiquitination.Frontiers in molecular biosciences · 2019Review
- Expression of WDR79 is associated withJournal of Cancer · 2019Article
- Haplotype and linkage disequilibrium of TP53-WRAP53 locus in Iranian-Azeri women with breast cancer.PloS one · 2019Article
- Tissue Expression Difference between mRNAs and lncRNAs.International journal of molecular sciences · 2018Article
- Programming of Cell Resistance to Genotoxic and Oxidative Stress.Biomedicines · 2018Review
- WRAP53β, survivin and p16INK4a expression as potential predictors of radiotherapy/chemoradiotherapy response in T2N0-T3N0 glottic laryngeal cancer.Oncology reports · 2017Article
- Specific genomic cues regulate Cajal body assembly.RNA biology · 2017Review
- Phosphorylation of the Cajal body protein WRAP53β by ATM promotes its involvement in the DNA damage response.RNA biology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Altered expression of the multifunctional protein WRAP53β (WD40 encoding RNA Antisense to p53), which targets repair factors to DNA double-strand breaks and factors involved in telomere elongation to Cajal bodies, is linked to carcinogenesis. While loss of WRAP53β function has been shown to disrupt processes regulated by this protein, the consequences of its overexpression remain unclear. Here we demonstrate that overexpression of WRAP53β disrupts the formation of and impairs the localization of coilin to Cajal bodies. At the same time, the function of this protein in the repair of DNA double-strand breaks is enhanced. Following irradiation, cells overexpressing WRAP53β exhibit more rapid clearance of phospho-histone H2AX (γH2AX), and more efficient homologous recombination and non-homologous end-joining, in association with fewer DNA breaks. Moreover, in these cells the ubiquitylation of damaged chromatin, which is known to facilitate the recruitment of repair factors and subsequent repair, is elevated. Knockdown of the ubiquitin ligase involved, ring-finger protein 8 (RNF8), which is recruited to DNA breaks by WRAP53β, attenuated this effect, suggesting that overexpression of WRAP53β leads to more rapid repair, as well as improved cell survival, by enhancing RNF8-mediated ubiquitylation at DNA breaks. Our present findings indicate that WRAP53β and RNF8 are rate-limiting factors in the repair of DNA double-strand breaks and raise the possibility that upregulation of WRAP53β may contribute to genomic stability in and survival of cancer cells.
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