Evidence map›Paper›PMID 27650961›Full record

ArticleCell cycle (Georgetown, Tex.)2016

Coronin 1B supports RhoA signaling at cell-cell junctions through Myosin II.

Rashmi Priya, Kenneth Wee, Srikanth Budnar, Guillermo A Gomez, Alpha S Yap, Magdalene Michael

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mobility and Invasion Related Gene Expression Patterns in Equine Sarcoid.Animals : an open access journal from MDPI · 2020
    Article
  7. Article
  8. Spatio-Temporal Regulation of RhoGTPases Signaling by Myosin II.Frontiers in cell and developmental biology · 2019
    Review
  9. Review
  10. Review
  11. 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

6 authors at 1 institution in 2 countries.

Rashmi Priyaa Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
Kenneth Weea Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
Srikanth Budnara Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
Guillermo A Gomeza Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
Alpha S Yapa Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
Magdalene Michaela Division of Cell Biology and Molecular Medicine, Program in Membrane Interface Biology, Institute for Molecular Bioscience, The University of Queensland, St. Lucia , Brisbane , Queensland , Australia.
University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-muscle myosin II (NMII) motor proteins are responsible for generating contractile forces inside eukaryotic cells. There is also a growing interest in the capacity for these motor proteins to influence cell signaling through scaffolding, especially in the context of RhoA GTPase signaling. We previously showed that NMIIA accumulation and stability within specific regions of the cell cortex, such as the zonula adherens (ZA), allows the formation of a stable RhoA signaling zone. Now we demonstrate a key role for Coronin 1B in maintaining this junctional pool of NMIIA, as depletion of Coronin 1B significantly compromised myosin accumulation and stability at junctions. The loss of junctional NMIIA, upon Coronin 1B knockdown, perturbed RhoA signaling due to enhanced junctional recruitment of the RhoA antagonist, p190B Rho GAP. This effect was blocked by the expression of phosphomimetic MRLC-DD, thus reinforcing the central role of NMII in regulating RhoA signaling.

Indexed as

Signal Transduction4-ButyrolactoneAcetogeninsActomyosinAdherens JunctionsCaco-2 CellsCadherinsEpithelial CellsGTPase-Activating ProteinsGuanosine TriphosphateHumansIntercellular JunctionsMCF-7 CellsModels, BiologicalMyosin Light ChainsNonmuscle Myosin Type IIA4-ButyrolactoneAcetogeninsActomyosinCadherinscoronin acetogeninGTPase-Activating ProteinsGuanosine TriphosphateMyosin Light ChainsNonmuscle Myosin Type IIArhoA GTP-Binding ProteinCoronin 1BFeedbackNMIIAp190BRhoA

Identifiers

PMID27650961
PMCPMC5134703
OpenAlexW2522378601

What OpenQuestion holds

Textmetadata
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.