ArticleCell cycle (Georgetown, Tex.)2015
A role for homologous recombination proteins in cell cycle regulation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 27 citations in OpenAlex.
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- Characterizing the evolutionary dynamics of cancer proliferation in single-cell clones with SPRINTER.Nature genetics · 2025Article
- Single-Cell Atlas of the Chinese Tongue SoleFrontiers in cell and developmental biology · 2022Article
- Prexasertib treatment induces homologous recombination deficiency and synergizes with olaparib in triple-negative breast cancer cells.Breast cancer research : BCR · 2019Article
- Homologous recombination and DNA repair mutations in patients treated with carboplatin and nab-paclitaxel for metastatic non-small cell lung cancer.Lung cancer (Amsterdam, Netherlands) · 2019Article
- TALEN-Mediated Gene Editing ofMolecular therapy. Methods & clinical development · 2019Article
- Overexpression of RAD51B predicts a preferable prognosis for non-small cell lung cancer patients.Oncotarget · 2017Article
- MAR-Mediated transgene integration into permissive chromatin and increased expression by recombination pathway engineering.Biotechnology and bioengineering · 2017Article
- Screening of Pesticides with the Potential of Inducing DSB and Successive Recombinational Repair.Journal of toxicology · 2017Article
- Valproic acid causes radiosensitivity of breast cancer cellsToxicology research · 2016Article
- Screening of Pleural Mesotheliomas for DNA-damage Repair Players by Digital Gene Expression Analysis Can Enhance Clinical Management of Patients Receiving Platin-Based Chemotherapy.Journal of Cancer · 2016Article
- Presence control of DNA repair controllers.Cell cycle (Georgetown, Tex.) · 2015Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells respond to DNA breaks, especially double-stranded breaks (DSBs), by activating the DNA damage response (DDR), which encompasses DNA repair and cell cycle checkpoint signaling. The DNA damage signal is transmitted to the checkpoint machinery by a network of specialized DNA damage-recognizing and signal-transducing molecules. However, recent evidence suggests that DNA repair proteins themselves may also directly contribute to the checkpoint control. Here, we investigated the role of homologous recombination (HR) proteins in normal cell cycle regulation in the absence of exogenous DNA damage. For this purpose, we used Chinese Hamster Ovary (CHO) cells expressing the Fluorescent ubiquitination-based cell cycle indicators (Fucci). Systematic siRNA-mediated knockdown of HR genes in these cells demonstrated that the lack of several of these factors alters cell cycle distribution, albeit differentially. The knock-down of MDC1, Rad51 and Brca1 caused the cells to arrest in the G2 phase, suggesting that they may be required for the G2/M transition. In contrast, inhibition of the other HR factors, including several Rad51 paralogs and Rad50, led to the arrest in the G1/G0 phase. Moreover, reduced expression of Rad51B, Rad51C, CtIP and Rad50 induced entry into a quiescent G0-like phase. In conclusion, the lack of many HR factors may lead to cell cycle checkpoint activation, even in the absence of exogenous DNA damage, indicating that these proteins may play an essential role both in DNA repair and checkpoint signaling.
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