Evidence map›Paper›PMID 29909276›Full record

ArticleCell systems2018

Quantitative Analysis Reveals that Actin and Src-Family Kinases Regulate Nuclear YAP1 and Its Export.

Nil Ege, Anna M Dowbaj, Ming Jiang, Michael Howell, Steven Hooper, Charles Foster, Robert P Jenkins, Erik Sahai

Open access · hybridAbstract read
In one paragraph

Article in Cell systems, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 136 citations in OpenAlex.

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31 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Nil EgeTumour Cell Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK; Cell and Developmental Biology Department, University College London, London WC1E 6BT, UK.
Anna M DowbajTumour Cell Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Ming JiangHigh Throughput Screening, The Francis Crick Institute, London NW1 1AT, UK.
Michael HowellHigh Throughput Screening, The Francis Crick Institute, London NW1 1AT, UK.
Steven HooperTumour Cell Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Charles FosterTranscription Laboratory, The Francis Crick Institute, London NW1 1AT, UK.
Robert P JenkinsTumour Cell Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK. Electronic address: robert.jenkins@crick.ac.uk.
Erik SahaiTumour Cell Biology Laboratory, The Francis Crick Institute, London NW1 1AT, UK. Electronic address: erik.sahai@crick.ac.uk.
The Francis Crick Institute · GBUniversity College London · GB

Funding

Cancer Research UK 15687Cancer Research UK FC001190Cancer Research UK FC001999Medical Research Council 520446Medical Research Council FC001144Medical Research Council FC001190Medical Research Council FC001999Wellcome Trust FC001144Wellcome Trust FC001190
6 · The paper itself

Abstract

The transcriptional regulator YAP1 is critical for the pathological activation of fibroblasts. In normal fibroblasts, YAP1 is located in the cytoplasm, while in activated cancer-associated fibroblasts, it is nuclear and promotes the expression of genes required for pro-tumorigenic functions. Here, we investigate the dynamics of YAP1 shuttling in normal and activated fibroblasts, using EYFP-YAP1, quantitative photobleaching methods, and mathematical modeling. Imaging of migrating fibroblasts reveals the tight temporal coupling of cell shape change and altered YAP1 localization. Both 14-3-3 and TEAD binding modulate YAP1 shuttling, but neither affects nuclear import. Instead, we find that YAP1 nuclear accumulation in activated fibroblasts results from Src and actomyosin-dependent suppression of phosphorylated YAP1 export. Finally, we show that nuclear-constrained YAP1, upon XPO1 depletion, remains sensitive to blockade of actomyosin function. Together, these data place nuclear export at the center of YAP1 regulation and indicate that the cytoskeleton can regulate YAP1 within the nucleus.

Indexed as

ActinsActive Transport, Cell NucleusAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell Line, TumorCell MovementCell NucleusCell ProliferationCytoplasmCytoskeletonDNA-Binding ProteinsFibroblastsGene Expression RegulationHumansMiceActinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsPhosphoproteinssrc-Family KinasesYap1 protein, mouseYAP-Signaling Proteinsactomyosin cytoskeletonfibroblastmathematical modelingnuclear exportphotobleachingSrc-family kinasesYAP1

Identifiers

PMID29909276
PMCPMC6035388
OpenAlexW2809358976

What OpenQuestion 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 OpenQuestion graph.