Evidence map›Paper›PMID 39080357›Full record

ArticleCommunications biology2024

Human T-cell receptor triggering requires inactivation of Lim kinase-1 by Slingshot-1 phosphatase.

Álvaro Gómez-Morón, Sergio Alegre-Gómez, Rocio Ramirez-Muñoz, Alicia Hernaiz-Esteban, Carlos Carrasco-Padilla, Camila Scagnetti, Óscar Aguilar-Sopeña, Marta García-Gil, Aldo Borroto, Raul Torres-Ruiz and 4 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

14 authors.

Álvaro Gómez-Morón *Department of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Sergio Alegre-Gómez *Department of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Rocio Ramirez-MuñozDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Alicia Hernaiz-EstebanDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Carlos Carrasco-PadillaDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Camila ScagnettiImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa, IIS-Princesa, UAM, 28006, Madrid, Spain.
Óscar Aguilar-SopeñaDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Marta García-GilDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
Aldo BorrotoCentro de Biología Molecular Severo Ochoa, Campus de Cantoblanco, 28049, Madrid, Spain.
Raul Torres-RuizMolecular Cytogenetics and Genome Editing Unit, Human Cancer Genetics Program, Centro Nacional de Investigaciones Oncológicas (CNIO), 28029, Madrid, Spain.
Sandra Rodriguez-PeralesMolecular Cytogenetics and Genome Editing Unit, Human Cancer Genetics Program, Centro Nacional de Investigaciones Oncológicas (CNIO), 28029, Madrid, Spain.ORCID 0000-0001-7221-3636
Francisco Sánchez-MadridImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa, IIS-Princesa, UAM, 28006, Madrid, Spain.
Noa Beatriz Martín-CófrecesImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa, IIS-Princesa, UAM, 28006, Madrid, Spain. noa.martin@salud.madrid.org.ORCID 0000-0003-0439-8979
Pedro Roda-NavarroDepartment of Immunology, Ophthalmology and ENT, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain. proda@ucm.es.ORCID 0000-0003-3799-8823

Funding

Comunidad de Madrid Y2018/BIO-5207_SINERGY_CAMMinistry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2020-115444GB-I00
6 · The paper itself

Abstract

Actin dynamics control early T-cell receptor (TCR) signalling during T-cell activation. However, the precise regulation of initial actin rearrangements is not completely understood. Here, we have investigated the regulatory role of the phosphatase Slingshot-1 (SSH1) in this process. Our data show that SSH1 rapidly polarises to nascent cognate synaptic contacts and later relocalises to peripheral F-actin networks organised at the mature immunological synapse. Knockdown of SSH1 expression by CRISPR/Cas9-mediated genome editing or small interfering RNA reveal a regulatory role for SSH1 in CD3ε conformational change, allowing Nck binding and proper downstream signalling and immunological synapse organisation. TCR triggering induces SSH1-mediated activation of actin dynamics through a mechanism mediated by Limk-1 inactivation. These data suggest that during early TCR activation, SSH1 is required for rapid F-actin rearrangements that mediate initial conformational changes of the TCR, integrin organisation and proximal signalling events for proper synapse organisation. Therefore, the SSH1 and Limk-1 axis is a key regulatory element for full T cell activation.

Indexed as

Lim KinasesPhosphoprotein PhosphatasesReceptors, Antigen, T-CellActinsHumansImmunological SynapsesJurkat CellsLymphocyte ActivationSignal TransductionT-LymphocytesActinsLIMK1 protein, humanLim KinasesPhosphoprotein PhosphatasesReceptors, Antigen, T-CellSSH1 protein, human

Identifiers

PMID39080357
PMCPMC11289303

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.