ReviewDNA repair2015
Historical perspective on the DNA damage response.
Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 58 citations in OpenAlex.
- Article
- AZD-7648, a DNA-PK Inhibitor, Induces DNA Damage, Apoptosis, and Cell Cycle Arrest in Chronic and Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2023Article
- Opi1-mediated transcriptional modulation orchestrates genotoxic stress response in budding yeast.Genetics · 2023Article
- SOS-independent bacterial DNA damage responses: diverse mechanisms, unifying function.Current opinion in microbiology · 2023Review
- Nanotechnology as a Tool for Optimizing Topical Photoprotective Formulations Containing Buriti Oil (Pharmaceuticals (Basel, Switzerland) · 2023Article
- The SMC-like RecN protein is at the crossroads of several genotoxic stress responses inFrontiers in microbiology · 2023Article
- The ataxia-telangiectasia mutated gene product regulates the cellular acid-labile sulfide fraction.DNA repair · 2022Article
- Eukaryotic stress-induced mutagenesis is limited by a local control of translesion synthesis.Nucleic acids research · 2022Article
- Bad Smells and Broken DNA: A Tale of Sulfur-Nucleic Acid Cooperation.Antioxidants (Basel, Switzerland) · 2021Review
- TARG1 protects against toxic DNA ADP-ribosylation.Nucleic acids research · 2021Article
- The Regulation of LexA on UV-Induced SOS Response inJournal of microbiology and biotechnology · 2021Article
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- Collateral Victim or Rescue Worker?-The Role of Histone Methyltransferases in DNA Damage Repair and Their Targeting for Therapeutic Opportunities in Cancer.Frontiers in cell and developmental biology · 2021Review
- The interaction of DNA repair factors ASCC2 and ASCC3 is affected by somatic cancer mutations.Nature communications · 2020Article
- WIP1 dephosphorylation of p27Cell cycle (Georgetown, Tex.) · 2020Article
- UBR5 interacts with the replication fork and protects DNA replication from DNA polymerase η toxicity.Nucleic acids research · 2019Article
- TET1 regulates DNA repair in human glial cells.Toxicology and applied pharmacology · 2019Article
- Carotenoids from UV-resistant Antarctic Microbacterium sp. LEMMJ01.Scientific reports · 2019Article
- Osteogenic differentiation of skeletal muscle progenitor cells is activated by the DNA damage response.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The DNA damage response (DDR) has been broadly defined as a complex network of cellular pathways that cooperate to sense and repair lesions in DNA. Multiple types of DNA damage, some natural DNA sequences, nucleotide pool deficiencies and collisions with transcription complexes can cause replication arrest to elicit the DDR. However, in practice, the term DDR as applied to eukaryotic/mammalian cells often refers more specifically to pathways involving the activation of the ATM (ataxia-telangiectasia mutated) and ATR (ATM-Rad3-related) kinases in response to double-strand breaks or arrested replication forks, respectively. Nevertheless, there are distinct responses to particular types of DNA damage that do not involve ATM or ATR. In addition, some of the aberrations that cause replication arrest and elicit the DDR cannot be categorized as direct DNA damage. These include nucleotide pool deficiencies, nucleotide sequences that can adopt non-canonical DNA structures, and collisions between replication forks and transcription complexes. The response to these aberrations can be called the genomic stress response (GSR), a term that is meant to encompass the sensing of all types of DNA aberrations together with the mechanisms involved in coping with them. In addition to fully functional cells, the consequences of processing genomic aberrations may include mutagenesis, genomic rearrangements and lethality.
Indexed as
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.