ArticleDNA repair2012
Recruitment and retention dynamics of RECQL5 at DNA double strand break sites.
Article in DNA repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Meta-analysis of DNA double-strand break response kinetics.Nucleic acids research · 2017Pooled it
- Review
- Senataxin and DNA-PKcs redundantly promote non-homologous end joining repair of DNA double strand breaks during V(D)J recombination.Science advances · 2025Article
- Expression of human RECQL5 in Saccharomyces cerevisiae causes transcription defects and transcription-associated genome instability.Molecular genetics and genomics : MGG · 2024Article
- Human RecQ Helicases in DNA Double-Strand Break Repair.Frontiers in cell and developmental biology · 2021Review
- Sweet Melody or Jazz? Transcription Around DNA Double-Strand Breaks.Frontiers in molecular biosciences · 2021Review
- Increased levels of RECQ5 shift DNA repair from canonical to alternative pathways.Nucleic acids research · 2018Article
- Differential RPA-1 and RAD-51 recruitment in vivo throughout the C. elegans germline, as revealed by laser microirradiation.Nucleic acids research · 2018Article
- Insights into the RecQ helicase mechanism revealed by the structure of the helicase domain of human RECQL5.Nucleic acids research · 2017Article
- JNK Phosphorylates SIRT6 to Stimulate DNA Double-Strand Break Repair in Response to Oxidative Stress by Recruiting PARP1 to DNA Breaks.Cell reports · 2016Article
- Clinicopathological and prognostic significance of RECQL5 helicase expression in breast cancers.Carcinogenesis · 2016Article
- Differential and Concordant Roles for Poly(ADP-Ribose) Polymerase 1 and Poly(ADP-Ribose) in Regulating WRN and RECQL5 Activities.Molecular and cellular biology · 2015Article
- RECQ helicase RECQL4 participates in non-homologous end joining and interacts with the Ku complex.Carcinogenesis · 2014Article
- Article
- Tumor suppressor RecQL5 controls recombination induced by DNA crosslinking agents.Biochimica et biophysica acta · 2014Article
- Molecular recognition by the KIX domain and its role in gene regulation.Nucleic acids research · 2014Review
- The RecQ helicase RECQL5 participates in psoralen-induced interstrand cross-link repair.Carcinogenesis · 2013Article
- DNA helicases involved in DNA repair and their roles in cancer.Nature reviews. Cancer · 2013Review
- RECQL5 plays co-operative and complementary roles with WRN syndrome helicase.Nucleic acids research · 2013Article
- Human RECQL5 participates in the removal of endogenous DNA damage.Molecular biology of the cell · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
RECQL5 is one of the five human RecQ helicases, involved in the maintenance of genomic integrity. While much insight has been gained into the function of the Werner (WRN) and Bloom syndrome proteins (BLM), little is known about RECQL5. We have analyzed the recruitment and retention dynamics of RECQL5 at laser-induced DNA double strand breaks (DSBs) relative to other human RecQ helicases. RECQL5-depleted cells accumulate persistent 53BP1 foci followed by γ-irradiation, indicating a potential role of RECQL5 in the processing of DSBs. Real time imaging of live cells using confocal laser microscopy shows that RECQL5 is recruited early to laser-induced DSBs and remains for a shorter duration than BLM and WRN, but persist longer than RECQL4. These studies illustrate the differential involvement of RecQ helicases in the DSB repair process. Mapping of domains within RECQL5 that are necessary for recruitment to DSBs revealed that both the helicase and KIX domains are required for DNA damage recognition and stable association of RECQL5 to the DSB sites. Previous studies have shown that MRE11 is essential for the recruitment of RECQL5 to the DSB sites. Here we show that the recruitment of RECQL5 does not depend on the exonuclease activity of MRE11 or on active transcription by RNA polymerase II, one of the prominent interacting partners of RECQL5. Also, the recruitment of RECQL5 to laser-induced damage sites is independent of the presence of other DNA damage signaling and repair proteins BLM, WRN and ATM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.