Evidence map›Paper›PMID 38019605›Full record

ArticleMolecular biology of the cell2024

Quaking isoforms cooperate to promote the mesenchymal phenotype.

Daniel P Neumann, Caroline A Phillips, Rachael Lumb, Helen M Palethorpe, Yesha Ramani, Brett G Hollier, Luke A Selth, Cameron P Bracken, Gregory J Goodall, Philip A Gregory

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biology of the cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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

10 authors at 3 institutions in 1 country.

Daniel P NeumannCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Caroline A PhillipsCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Rachael LumbCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Helen M PalethorpeCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Yesha RamaniCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Brett G HollierAustralian Prostate Cancer Research Centre - Queensland, Centre for Genomics and Personalised Health, Faculty of Health, School of Biomedical Sciences, Queensland University of Technology, Translational Research Institute, Brisbane, Queensland 4102, Australia.
Luke A SelthFlinders Health and Medical Research Institute and Freemasons Centre for Male Health and Wellbeing, Flinders University, Bedford Park, South Australia 5042, Australia.
Cameron P BrackenCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Gregory J GoodallCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
Philip A GregoryCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia 5000, Australia.
South Australia Pathology · AUFlinders University · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The RNA-binding protein Quaking (QKI) has widespread effects on mRNA regulation including alternative splicing, stability, translation, and localization of target mRNAs. Recently, QKI was found to be induced during epithelial-mesenchymal transition (EMT), where it promotes a mesenchymal alternative splicing signature that contributes to the mesenchymal phenotype. QKI is itself alternatively spliced to produce three major isoforms, QKI-5, QKI-6, and QKI-7. While QKI-5 is primarily localized to the nucleus where it controls mesenchymal splicing during EMT, the functions of the two predominantly cytoplasmic isoforms, QKI-6 and QKI-7, in this context remain uncharacterized. Here we used CRISPR-mediated depletion of QKI in a human mammary epithelial cell model of EMT and studied the effects of expressing the QKI isoforms in isolation and in combination. QKI-5 was required to induce mesenchymal morphology, while combined expression of QKI-5 with either QKI-6 or QKI-7 further enhanced mesenchymal morphology and cell migration. In addition, we found that QKI-6 and QKI-7 can partially localize to the nucleus and contribute to alternative splicing of QKI target genes. These findings indicate that the QKI isoforms function in a dynamic and cooperative manner to promote the mesenchymal phenotype.

Indexed as

Alternative SplicingRNA SplicingHumansPhenotypeProtein IsoformsRNA, MessengerProtein IsoformsRNA, Messenger

Identifiers

PMID38019605
PMCPMC10881146
OpenAlexW4389132517

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.