ArticleCell division2006
Tying the loose ends together in DNA double strand break repair with 53BP1.
Article in Cell division, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
51 citing papers in PubMed, 77 citations in OpenAlex.
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Integrating Vascular Phenotypic and Proteomic Analysis in an Open Microfluidic Platform.ACS nano · 2024Article
- Chromatin Organization after High-LET Irradiation Revealed by Super-Resolution STED Microscopy.International journal of molecular sciences · 2024Article
- Transient inhibition of 53BP1 increases the frequency of targeted integration in human hematopoietic stem and progenitor cells.Nature communications · 2024Article
- Diabetes-associated breast cancer is molecularly distinct and shows a DNA damage repair deficiency.JCI insight · 2023Article
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- CST in maintaining genome stability: Beyond telomeres.DNA repair · 2021Review
- Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1.Journal of Zhejiang University. Science. B · 2021Review
- The end protection problem-an unexpected twist in the tail.Genes & development · 2021Article
- Resveratrol inhibits apoptosis by increase in the proportion of chondrocytes in the S phase of cell cycle in articular cartilage of ACLT plus Mmx rats.Saudi journal of biological sciences · 2019Article
- Article
- Generating and repairing genetically programmed DNA breaks during immunoglobulin class switch recombination.F1000Research · 2018Review
- 53BP1 Contributes toJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- The FEN1 L209P mutation interferes with long-patch base excision repair and induces cellular transformation.Oncogene · 2017Article
- The actin depolymerizing factor (ADF)/cofilin signaling pathway and DNA damage responses in cancer.International journal of molecular sciences · 2015Review
- Differential regulation of S-region hypermutation and class-switch recombination by noncanonical functions of uracil DNA glycosylase.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- 53BP1: pro choice in DNA repair.Trends in cell biology · 2014Review
- Chemotherapeutic compounds targeting the DNA double-strand break repair pathways: the good, the bad, and the promising.Frontiers in oncology · 2014Review
- Regulation and roles of Cdc7 kinase under replication stress.Cell cycle (Georgetown, Tex.) · 2014Review
- Double-strand break repair: 53BP1 comes into focus.Nature reviews. Molecular cell biology · 2014Review
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
To maintain genomic stability and ensure the fidelity of chromosomal transmission, cells respond to various forms of genotoxic stress, including DNA double-stranded breaks (DSBs), through the activation of DNA damage response signaling networks. In response to DSBs as induced by ionizing radiation (IR), during DNA replication, or through immunoglobulin heavy chain (IgH) rearrangements in B cells of lymphoid origin, the phosphatidyl inositol-like kinase (PIK) kinases ATM (mutated in ataxia telangiectasia), ATR (ATM and Rad3-related kinase), and the DNA-dependent protein kinase (DNA-PK) activate signaling pathways that lead to DSB repair. DSBs are repaired by either of two major, non-mutually exclusive pathways: homologous recombination (HR) that utilizes an undamaged sister chromatid template (or homologous chromosome) and non- homologous end joining (NHEJ), an error prone mechanism that processes and joins broken DNA ends through the coordinated effort of a small set of ubiquitous factors (DNA-PKcs, Ku70, Ku80, artemis, Xrcc4/DNA lig IV, and XLF/Cernunnos). The PIK kinases phosphorylate a variety of effector substrates that propagate the DNA damage signal, ultimately resulting in various biological outputs that influence cell cycle arrest, transcription, DNA repair, and apoptosis. A variety of data has revealed a critical role for p53-binding protein 1 (53BP1) in the cellular response to DSBs including various aspects of p53 function. Importantly, 53BP1 plays a major role in suppressing translocations, particularly in B and T cells. This report will review past experiments and current knowledge regarding the role of 53BP1 in the DNA damage response.
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.