ArticleMolecular and cellular biology2018
53BP1 Mediates ATR-Chk1 Signaling and Protects Replication Forks under Conditions of Replication Stress.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 67 citations in OpenAlex.
- Not only as a Cullin3 ligase adaptor, SPOP may also act as a molecular bridge.Genes & diseases · 2027Review
- Article
- MDC1 counteracts replication fork reversal and mediates chemosensitivity in BRCA1/2-deficient tumors.Oncogene · 2026Article
- Medicinal chemistry breakthroughs on ATM, ATR, and DNA-PK inhibitors as prospective cancer therapeutics.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- Genetic modeling of ELP1-associated Sonic hedgehog medulloblastoma identifies MDM2 as a selective therapeutic target.Cancer cell · 2025Article
- ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer.Nature communications · 2025Article
- 53BP1-the 'Pandora's box' of genome integrity.DNA repair · 2024Review
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Autocorrelation analysis of a phenotypic screen reveals hidden drug activity.Scientific reports · 2024Article
- RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication.The Journal of clinical investigation · 2024Article
- Liquid-liquid phase separation in DNA double-strand breaks repair.Cell death & disease · 2023Review
- Replication stress and defective checkpoints make fallopian tube epithelial cells putative drivers of high-grade serous ovarian cancer.Cell reports · 2023Article
- Wnt3a signaling with serum supply induces replication stress in cultured cells.Biochemistry and biophysics reports · 2023Article
- Preliminary Study on 53BP1-Mediated DNA Double-Strand Break Response in Spermatogonial Stem Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- The organizer of chromatin topology RIF1 ensures cellular resilience to DNA replication stress.Life science alliance · 2023Article
- DNA Damage Response Mechanisms in Head and Neck Cancer: Significant Implications for Therapy and Survival.International journal of molecular sciences · 2023Review
- Review
- MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner.Nature communications · 2022Article
- Article
- Nitrogen Mustard Alkylates and Cross-Links p53 in Human Keratinocytes.Chemical research in toxicology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Complete replication of the genome is an essential prerequisite for normal cell division, but a variety of factors can block the replisome, triggering replication stress and potentially causing mutation or cell death. The cellular response to replication stress involves recruitment of proteins to stabilize the replication fork and transmit a stress signal to pause the cell cycle and allow fork restart. We find that the ubiquitously expressed DNA damage response factor 53BP1 is required for the normal response to replication stress. Using primary,
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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.