ArticleCell cycle (Georgetown, Tex.)2014
Npl3, a new link between RNA-binding proteins and the maintenance of genome integrity.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- Npl3 stabilizes R-loops at telomeres to prevent accelerated replicative senescence.EMBO reports · 2020Article
- Splicing events in the control of genome integrity: role of SLU7 and truncated SRSF3 proteins.Nucleic acids research · 2019Article
- Distinct Functions of the Cap-Binding Complex in Stimulation of Nuclear mRNA Export.Molecular and cellular biology · 2019Article
- The Yeast DNA Damage Checkpoint Kinase Rad53 Targets the Exoribonuclease, Xrn1.G3 (Bethesda, Md.) · 2018Article
- Cis- and Trans-Modifiers of Repeat Expansions: Blending Model Systems with Human Genetics.Trends in genetics : TIG · 2018Review
- Profiling DNA damage-induced phosphorylation in budding yeast reveals diverse signaling networks.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Double-strand break repair deficiency in NONO knockout murine embryonic fibroblasts and compensation by spontaneous upregulation of the PSPC1 paralog.Nucleic acids research · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mRNA is co-transcriptionally bound by a number of RNA-binding proteins (RBPs) that contribute to its processing and formation of an export-competent messenger ribonucleoprotein particle (mRNP). In the last few years, increasing evidence suggests that RBPs play a key role in preventing transcription-associated genome instability. Part of this instability is mediated by the accumulation of co-transcriptional R loops, which may impair replication fork (RF) progression due to collisions between transcription and replication machineries. In addition, some RBPs have been implicated in DNA repair and/or the DNA damage response (DDR). Recently, the Npl3 protein, one of the most abundant heterogeneous nuclear ribonucleoproteins (hnRNPs) in yeast, has been shown to prevent transcription-associated genome instability and accumulation of RF obstacles, partially associated with R-loop formation. Interestingly, Npl3 seems to have additional functions in DNA repair, and npl3∆ mutants are highly sensitive to genotoxic agents, such as the antitumor drug trabectedin. Here we discuss the role of Npl3 in particular, and RBPs in general, in the connection of transcription with replication and genome instability, and its effect on the DDR.
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.