Evidence map›Paper›PMID 27763814›Full record

ArticleRNA biology2017

The RNA-binding landscape of RBM10 and its role in alternative splicing regulation in models of mouse early development.

Julie Rodor, David R FitzPatrick, Eduardo Eyras, Javier F Cáceres

Open access · hybridAbstract read
In one paragraph

Article in RNA biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Splicing factor RBM10 loss fuels thyroid cancer metastasis.The Journal of experimental medicine · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Zoological research · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. RNA-binding proteins in human genetic disease.Nature reviews. Genetics · 2021
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Julie Rodora Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital , Edinburgh , EH4 2XU , UK.
David R FitzPatricka Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital , Edinburgh , EH4 2XU , UK.
Eduardo Eyrasb Computational Genomics Group, Universitat Pompeu Fabra , E08003 , Barcelona , Spain.
Javier F Cáceresa Medical Research Council Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital , Edinburgh , EH4 2XU , UK.
Medical Research Council · GBPompeu Fabra University · ESWestern General Hospital · GB

Funding

Medical Research Council MC_PC_U127561093Medical Research Council MC_PC_U127584479Wellcome Trust 095518/Z/11/Z
6 · The paper itself

Abstract

Mutations in the RNA-binding protein, RBM10, result in a human syndromic form of cleft palate, termed TARP syndrome. A role for RBM10 in alternative splicing regulation has been previously demonstrated in human cell lines. To uncover the cellular functions of RBM10 in a cell line that is relevant to the phenotype observed in TARP syndrome, we used iCLIP to identify its endogenous RNA targets in a mouse embryonic mandibular cell line. We observed that RBM10 binds to pre-mRNAs with significant enrichment in intronic regions, in agreement with a role for this protein in pre-mRNA splicing. In addition to protein-coding transcripts, RBM10 also binds to a variety of cellular RNAs, including non-coding RNAs, such as spliceosomal small nuclear RNAs, U2 and U12. RNA-seq was used to investigate changes in gene expression and alternative splicing in RBM10 KO mouse mandibular cells and also in mouse ES cells. We uncovered a role for RBM10 in the regulation of alternative splicing of common transcripts in both cell lines but also identified cell-type specific events. Importantly, those pre-mRNAs that display changes in alternative splicing also contain RBM10 iCLIP tags, suggesting a direct role of RBM10 in these events. Finally, we show that depletion of RBM10 in mouse ES cells leads to proliferation defects and to gross alterations in their differentiation potential. These results demonstrate a role for RBM10 in the regulation of alternative splicing in two cell models of mouse early development and suggests that mutations in RBM10 could lead to splicing changes that affect normal palate development and cause human disease.

Indexed as

Alternative SplicingGene Expression RegulationAnimalsBinding SitesChromosome MappingEmbryonic DevelopmentEmbryonic Stem CellsFemaleGene Knockout TechniquesGenome-Wide Association StudyHigh-Throughput Nucleotide SequencingMaleMiceMolecular Sequence AnnotationNucleotide MotifsPhenotypeRBM10 protein, mouseRNA-Binding ProteinsRNA, MessengerRNA, Small NuclearAlternative splicingiCLIPmandibular cell lineRBM10RNA-binding proteinsstem cellsTARP syndrome

Identifiers

PMID27763814
PMCPMC5270529
OpenAlexW2536702968

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.