Evidence map›Paper›PMID 37162507›Full record

ArticleeLife2023

ARPC5 isoforms and their regulation by calcium-calmodulin-N-WASP drive distinct Arp2/3-dependent actin remodeling events in CD4 T cells.

Lopamudra Sadhu, Nikolaos Tsopoulidis, Md Hasanuzzaman, Vibor Laketa, Michael Way, Oliver T Fackler

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
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  5. Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025
    Review
  6. Article
  7. Article
  8. The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025
    Review
  9. Article
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  12. Review
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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 2 institutions in 2 countries.

Lopamudra SadhuDepartment of Infectious Diseases, Integrative Virology, University Hospital Heidelberg, Heidelberg, Germany.
Nikolaos TsopoulidisDepartment of Infectious Diseases, Integrative Virology, University Hospital Heidelberg, Heidelberg, Germany.
Md HasanuzzamanDepartment of Infectious Diseases, Integrative Virology, University Hospital Heidelberg, Heidelberg, Germany.
Vibor LaketaDepartment of Infectious Diseases, Virology, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-9472-2738
Michael WayCellular Signalling and Cytoskeletal Function Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0001-7207-2722
Oliver T FacklerDepartment of Infectious Diseases, Integrative Virology, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0003-2982-4209
Heidelberg University · DEThe Francis Crick Institute · GB

Funding

European Research Council 810207Medical Research CouncilWellcome Trust CC2096
6 · The paper itself

Abstract

CD4 T cell activation induces nuclear and cytoplasmic actin polymerization via the Arp2/3 complex to activate cytokine expression and strengthen T cell receptor (TCR) signaling. Actin polymerization dynamics and filament morphology differ between nucleus and cytoplasm. However, it is unclear how the Arp2/3 complex mediates distinct nuclear and cytoplasmic actin polymerization in response to a common stimulus. In humans, the ARP3, ARPC1, and ARPC5 subunits of the Arp2/3 complex exist as two different isoforms, resulting in complexes with different properties. Here, we show that the Arp2/3 subunit isoforms ARPC5 and ARPC5L play a central role in coordinating distinct actin polymerization events in CD4 T cells. While ARPC5L is heterogeneously expressed in individual CD4 T cells, it specifically drives nuclear actin polymerization upon T cell activation. In contrast, ARPC5 is evenly expressed in CD4 T cell populations and is required for cytoplasmic actin dynamics. Interestingly, nuclear actin polymerization triggered by a different stimulus, DNA replication stress, specifically requires ARPC5 but not ARPC5L. TCR signaling but not DNA replication stress induces nuclear actin polymerization via nuclear calcium-calmodulin signaling and N-WASP. Diversity in the molecular properties and individual expression patterns of ARPC5 subunit isoforms thus tailors Arp2/3-mediated actin polymerization to different physiological stimuli.

Indexed as

ActinsCalmodulinActin-Related Protein 2Actin-Related Protein 2-3 ComplexActin-Related Protein 3CalciumCD4-Positive T-LymphocytesHumansProtein IsoformsReceptors, Antigen, T-CellActin-Related Protein 2Actin-Related Protein 2-3 ComplexActin-Related Protein 3ActinsACTR2 protein, humanACTR3 protein, humanARPC5 protein, humanCalciumCalmodulinProtein IsoformsReceptors, Antigen, T-CellArp2/3 complexCD4 T cell activationDNA replication stresshumanimmunologyinflammationnuclear F-actin

Identifiers

PMID37162507
PMCPMC10171864
OpenAlexW4376132844

What OpenQuestion holds

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LicenceCC BY
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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.