ReviewRNA biology2018
Modulating the expression of Chtop, a versatile regulator of gene-specific transcription and mRNA export.
Review in RNA biology, 2018. 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
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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
8 citing papers in PubMed, 19 citations in OpenAlex.
- High-throughput mapping of modular regulatory domains in human RNA-binding proteins.Cell systems · 2026Article
- Data augmentation based on the WGAN-GP with data block to enhance the prediction of genes associated with RNA methylation pathways.Scientific reports · 2024Article
- Deregulated circRNAs in Epithelial Ovarian Cancer With Activity in PreclinicalCancer genomics & proteomics · 2024Review
- TREX tetramer disruption alters RNA processing necessary for corticogenesis in THOC6 Intellectual Disability Syndrome.Nature communications · 2024Article
- Article
- Review
- CircHIPK2 Contributes to DDP Resistance and Malignant Behaviors of DDP-Resistant Ovarian Cancer Cells Both in vitro and in vivo Through circHIPK2/miR-338-3p/CHTOP ceRNA Pathway.OncoTargets and therapy · 2021Article
- Epigenetic dynamics in cancer stem cell dormancy.Cancer metastasis reviews · 2020Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chtop binds competitively to the arginine methyltransferases PRMT1 and PRMT5, thereby promoting the asymmetric or symmetric methylation of arginine residues, respectively. In cooperation with PRMT1, Chtop activates transcription of certain gene groups, such as the estrogen-inducible genes in breast cancer cells, the 5-hydroxymethylcytosine-modified genes involved in glioblastomagenesis, or the Zbp-89-dependent genes in erythroleukemia cells. Chtop also represses expression of the fetal γ-globin gene. In addition, Chtop is a component of the TREX complex that links transcription elongation to mRNA export. The regulation of Chtop expression is, therefore, a key process during the expression of certain gene groups and pathogenesis of certain diseases. Our recent study revealed that cellular levels of Chtop are strictly autoregulated by a mechanism involving intron retention and nonsense-mediated mRNA decay. Here, we summarize roles of Chtop in gene-specific expression and highlight our recent findings concerning the autoregulation of Chtop.
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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 Socratic graph.