ArticleInternational journal of proteomics2011
Phosphorylation: the molecular switch of double-strand break repair.
Article in International journal of proteomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- Rs12516 A allele elevates the risk of colorectal cancer via functional CeRNA network of BDNF-AS, miR-4704-5p and BRCA1.BMC cancer · 2026Article
- Site-specific genotoxicity of rubiadin: localization and histopathological changes in the kidneys of rats.Archives of toxicology · 2023Article
- Maintaining Genome Integrity: Protein Kinases and Phosphatases Orchestrate the Balancing Act of DNA Double-Strand Breaks Repair in Cancer.International journal of molecular sciences · 2023Review
- Article
- PARP-1 inhibitors enhance the chemosensitivity of leukemia cells by attenuating NF-кB pathway activity and DNA damage response induced by IdarubicinActa biochimica et biophysica Sinica · 2022Article
- Phosphorylation of TRIP13 at Y56 induces radiation resistance but sensitizes head and neck cancer to cetuximab.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Gold Nanoparticles as a Potent Radiosensitizer: A Transdisciplinary Approach from Physics to Patient.Cancers · 2020Review
- TIP60 K430 SUMOylation attenuates its interaction with DNA-PKcs in S-phase cells: Facilitating homologous recombination and emerging target for cancer therapy.Science advances · 2020Article
- Co-inhibition of Pol η and ATR sensitizes cisplatin-resistant non-small cell lung cancer cells to cisplatin by impeding DNA damage repair.Acta pharmacologica Sinica · 2018Article
- Protein phosphatase 1 and phosphatase 1 nuclear targeting subunit-dependent regulation of DNA-dependent protein kinase and non-homologous end joining.Nucleic acids research · 2017Article
- A critical role for topoisomerase IIb and DNA double strand breaks in transcription.Transcription · 2016Article
- Phosphorylation-Dependent Regulation of the DNA Damage Response of Adaptor Protein KIBRA in Cancer Cells.Molecular and cellular biology · 2016Article
- Enhanced susceptibility of ovaries from obese mice to 7,12-dimethylbenz[a]anthracene-induced DNA damage.Toxicology and applied pharmacology · 2014Article
- FUS is phosphorylated by DNA-PK and accumulates in the cytoplasm after DNA damage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- ATM increases activation-induced cytidine deaminase activity at downstream S regions during class-switch recombination.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Epstein-Barr virus essential antigen EBNA3C attenuates H2AX expression.Journal of virology · 2014Article
- 7,12-Dimethylbenz[a]anthracene exposure induces the DNA repair response in neonatal rat ovaries.Toxicology and applied pharmacology · 2013Article
- FANCD2 regulates BLM complex functions independently of FANCI to promote replication fork recovery.Nucleic acids research · 2013Article
- BRCA1-Ku80 protein interaction enhances end-joining fidelity of chromosomal double-strand breaks in the G1 phase of the cell cycle.The Journal of biological chemistry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Repair of double-stranded breaks (DSBs) is vital to maintaining genomic stability. In mammalian cells, DSBs are resolved in one of the following complex repair pathways: nonhomologous end-joining (NHEJ), homologous recombination (HR), or the inclusive DNA damage response (DDR). These repair pathways rely on factors that utilize reversible phosphorylation of proteins as molecular switches to regulate DNA repair. Many of these molecular switches overlap and play key roles in multiple pathways. For example, the NHEJ pathway and the DDR both utilize DNA-PK phosphorylation, whereas the HR pathway mediates repair with phosphorylation of RPA2, BRCA1, and BRCA2. Also, the DDR pathway utilizes the kinases ATM and ATR, as well as the phosphorylation of H2AX and MDC1. Together, these molecular switches regulate repair of DSBs by aiding in DSB recognition, pathway initiation, recruitment of repair factors, and the maintenance of repair mechanisms.
Identifiers
What OpenQuestion holds
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.