ArticleFrontiers in genetics2012
Posttranscriptional regulation of gene expression-adding another layer of complexity to the DNA damage response.
Article in Frontiers in genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 39 citations in OpenAlex.
- Transcription-wide impact by RESCUE-induced off-target single-nucleotide variants in mammalian cells.Journal of molecular cell biology · 2023Article
- MDF is a conserved splicing factor and modulates cell division and stress response inLife science alliance · 2023Article
- The transcription factor c-Jun inhibits RBM39 to reprogram pre-mRNA splicing during genotoxic stress.Nucleic acids research · 2022Article
- ADAR-mediated RNA editing of DNA:RNA hybrids is required for DNA double strand break repair.Nature communications · 2021Article
- The evolving complexity of DNA damage foci: RNA, condensates and chromatin in DNA double-strand break repair.DNA repair · 2021Review
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- Transcriptional responses to DNA damage.DNA repair · 2019Review
- Article
- Maintenance of genome stability: the unifying role of interconnections between the DNA damage response and RNA-processing pathways.Current genetics · 2018Review
- Inhibition of IRES-dependent translation of caspase-2 by HuR confers chemotherapeutic drug resistance in colon carcinoma cells.Oncotarget · 2018Article
- Tia1 dependent regulation of mRNA subcellular location and translation controls p53 expression in B cells.Nature communications · 2017Article
- MicroRNA and Transcription Factor: Key Players in Plant Regulatory Network.Frontiers in plant science · 2017Review
- Classical non-homologous end-joining pathway utilizes nascent RNA for error-free double-strand break repair of transcribed genes.Nature communications · 2016Article
- Serial interactome capture of the human cell nucleus.Nature communications · 2016Article
- C1D family proteins in coordinating RNA processing, chromosome condensation and DNA damage response.Cell division · 2016Review
- The RNA Splicing Response to DNA Damage.Biomolecules · 2015Review
- The interplay between DNA damage response and RNA processing: the unexpected role of splicing factors as gatekeepers of genome stability.Frontiers in genetics · 2015Article
- MicroRNAs Used in Combination with Anti-Cancer Treatments Can Enhance Therapy Efficacy.Mini reviews in medicinal chemistry · 2015Review
- Article
- MicroRNAs in the DNA Damage/Repair Network and Cancer.International journal of genomics · 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
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In response to DNA damage, cells activate a complex, kinase-based signaling network to arrest the cell cycle and allow time for DNA repair, or, if the extend of damage is beyond repair capacity, induce apoptosis. This signaling network, which is collectively referred to as the DNA damage response (DDR), is primarily thought to consist of two components-a rapid phosphorylation-driven signaling cascade that results in immediate inhibition of Cdk/cyclin complexes and a delayed transcriptional response that promotes a prolonged cell cycle arrest through the induction of Cdk inhibitors, such as p21. In recent years a third layer of complexity has emerged that involves potent posttranscriptional regulatory mechanisms that control the cellular response to DNA damage. Although much has been written on the relevance of the DDR in cancer and on the post-transcriptional role of microRNAs (miRs) in cancer, the post-transcriptional regulation of the DDR by non-coding RNAs and RNA-binding proteins (RBPs) still remains elusive in large parts. Here, we review the recent developments in this exciting new area of research in the cellular response to genotoxic stress. We put specific emphasis on the role of RBPs and the control of their function through DNA damage-activated protein kinases.
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.