ReviewDNA repair2009
14-3-3 proteins, FHA domains and BRCT domains in the DNA damage response.
Review in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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
88 citing papers in PubMed, 146 citations in OpenAlex.
- Fragment-based discovery of TopBP1 inhibitors integrated with AI-driven molecular docking.Magnetic resonance letters · 2026Article
- PARP4 ADP-ribosylates PIDD1 to complete a phospho/SUMO/PAR-ylation cascade that orchestrates PIDDosome assembly.Science advances · 2026Article
- TIPIN coordinates ATM-dependent checkpoint and NF-κB signaling to counteract DNA replication damage from topoisomerase inhibition.Communications biology · 2025Article
- Transcriptomic analysis reveals lung cancer and subtype-specific alternative splicing biomarkers regulated by RNA-binding proteins.Molecular therapy. Nucleic acids · 2025Article
- Breast cancer gene-1 (BRCA1) potentiates maladaptive repair after kidney injury.The Journal of experimental medicine · 2025Article
- NBS1 dePARylation by NUDT16 is critical for DNA double-strand break repair.Molecular and cellular biochemistry · 2025Article
- Effects of high-altitude environments on intervertebral disc degeneration and transcriptome profiling of the nucleus pulposus.Frontiers in cell and developmental biology · 2025Article
- SART1 modulates poly-(ADP-ribose) chain accumulation and PARP1 chromatin localization.iScience · 2024Article
- Target-based drug discovery: Applications of fluorescence techniques in high throughput and fragment-based screening.Heliyon · 2024Review
- Forkhead-associated phosphopeptide binding domain 1 (FHAD1) deficiency impaired murine sperm motility.PeerJ · 2024Article
- Article
- BRCT Domains: Structure, Functions, and Implications in Disease-New Therapeutic Targets for Innovative Drug Discovery against Infections.Pharmaceutics · 2023Review
- Hybrid-seq deciphers the complex transcriptional profile of the humanRNA biology · 2023Article
- The Breast Cancer Protooncogenes HER2, BRCA1 and BRCA2 and Their Regulation by the iNOS/NOS2 Axis.Antioxidants (Basel, Switzerland) · 2022Review
- DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway.Science signaling · 2022Article
- TCF19 Impacts a Network of Inflammatory and DNA Damage Response Genes in the Pancreatic β-Cell.Metabolites · 2021Article
- Predicted Cellular Interactors of the Endogenous Retrovirus-K Integrase Enzyme.Microorganisms · 2021Article
- Evolutionary crossroads of cell signaling: PP1 and PP2A substrate sites in intrinsically disordered regions.Biochemical Society transactions · 2021Review
- Clinical use and mechanisms of resistance for PARP inhibitors in homologous recombination-deficient cancers.Translational oncology · 2021Review
- Phosphoproteomic Analysis Reveals Rio1-Related Protein Phosphorylation Changes in Response to UV Irradiation inFrontiers in microbiology · 2020Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The DNA damage response depends on the concerted activity of protein serine/threonine kinases and modular phosphoserine/threonine-binding domains to relay the damage signal and recruit repair proteins. The PIKK family of protein kinases, which includes ATM/ATR/DNA-PK, preferentially phosphorylate Ser-Gln sites, while their basophilic downstream effecter kinases, Chk1/Chk2/MK2 preferentially phosphorylate hydrophobic-X-Arg-X-X-Ser/Thr-hydrophobic sites. A subset of tandem BRCT domains act as phosphopeptide binding modules that bind to ATM/ATR/DNA-PK substrates after DNA damage. Conversely, 14-3-3 proteins interact with substrates of Chk1/Chk2/MK2. FHA domains have been shown to interact with substrates of ATM/ATR/DNA-PK and CK2. In this review we consider how substrate phosphorylation together with BRCT domains, FHA domains and 14-3-3 proteins function to regulate ionizing radiation-induced nuclear foci and help to establish the G(2)/M checkpoint. We discuss the role of MDC1 a molecular scaffold that recruits early proteins to foci, such as NBS1 and RNF8, through distinct phosphodependent interactions. In addition, we consider the role of 14-3-3 proteins and the Chk2 FHA domain in initiating and maintaining cell cycle arrest.
Indexed as
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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.