Evidence map›Paper›PMID 26291837›Full record

ReviewBiochemistry and cell biology = Biochimie et biologie cellulaire2016

Connecting the dots: chromatin and alternative splicing in EMT.

Jessica A Warns, James R Davie, Archana Dhasarathy

Open access · greenAbstract readReview
In one paragraph

Review in Biochemistry and cell biology = Biochimie et biologie cellulaire, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024
    Review
  2. Article
  3. Article
  4. Working a second job: Cell adhesion proteins that moonlight in the nucleus.Frontiers in cell and developmental biology · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. The determinants of alternative RNA splicing in human cells.Molecular genetics and genomics : MGG · 2017
    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

3 authors at 2 institutions in 2 countries.

Jessica A Warnsa Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, 501 N. Columbia Road Stop 9061, Grand Forks, ND 58202-9061, USA.
James R Davieb Children's Hospital Research Institute of Manitoba, John Buhler Research Centre, Winnipeg, Manitoba R3E 3P4, Canada.
Archana Dhasarathya Department of Basic Sciences, University of North Dakota School of Medicine and Health Sciences, 501 N. Columbia Road Stop 9061, Grand Forks, ND 58202-9061, USA.
University of North Dakota · USChildren's Hospital Research Institute of Manitoba · CA

Funding

The role of class IIa Hdac in regulating cell fate choice in early cortical development.P20GM104360 · NIGMS · UNIVERSITY OF NORTH DAKOTA · PI VAUGHAN, ROXANNE A · 2013 to 2023
$21.1M
NIGMS NIH HHS 5P20GM104360NIGMS NIH HHS P20 GM104360
6 · The paper itself

Abstract

Nature has devised sophisticated cellular machinery to process mRNA transcripts produced by RNA Polymerase II, removing intronic regions and connecting exons together, to produce mature RNAs. This process, known as splicing, is very closely linked to transcription. Alternative splicing, or the ability to produce different combinations of exons that are spliced together from the same genomic template, is a fundamental means of regulating protein complexity. Similar to transcription, both constitutive and alternative splicing can be regulated by chromatin and its associated factors in response to various signal transduction pathways activated by external stimuli. This regulation can vary between different cell types, and interference with these pathways can lead to changes in splicing, often resulting in aberrant cellular states and disease. The epithelial to mesenchymal transition (EMT), which leads to cancer metastasis, is influenced by alternative splicing events of chromatin remodelers and epigenetic factors such as DNA methylation and non-coding RNAs. In this review, we will discuss the role of epigenetic factors including chromatin, chromatin remodelers, DNA methyltransferases, and microRNAs in the context of alternative splicing, and discuss their potential involvement in alternative splicing during the EMT process.

Indexed as

Alternative SplicingChromatin Assembly and DisassemblyChromatinDNA MethylationEpithelial-Mesenchymal TransitionExonsHistone CodeHumansIntronsNeoplasmsNucleosomesRNA, MessengerRNA Polymerase IIRNA PrecursorsRNA, UntranslatedSignal TransductionChromatinNucleosomesRNA, MessengerRNA Polymerase IIRNA PrecursorsRNA, Untranslatedalternative splicingcancerchromatinchromatineEMTepigeneticsépigénétiqueépissage alternatifTEM

Identifiers

PMID26291837
PMCPMC4704998
OpenAlexW1962512322

What OpenQuestion holds

Textmetadata
LicenceTDM
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.