Evidence map›Paper›PMID 37520527›Full record

ArticleFrontiers in immunology2023

End-binding protein 1 regulates the metabolic fate of CD4

Álvaro Gómez-Morón, Silvia Requena, Clara Pertusa, Marta Lozano-Prieto, Diego Calzada-Fraile, Camila Scagnetti, Inés Sánchez-García, Ana Adela Calero-García, Manuel Izquierdo, Noa B Martín-Cófreces

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. 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 4 institutions in 1 country.

Álvaro Gómez-MorónImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Silvia RequenaImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Clara PertusaImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Marta Lozano-PrietoImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Diego Calzada-FraileVascular Pathophysiology, Laboratory of Intercellular Communication, Fundación Centro Nacional de Investigaciones Cardiovasculares-Carlos III (CNIC), Madrid, Spain.
Camila ScagnettiImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Inés Sánchez-GarcíaImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Ana Adela Calero-GarcíaNeumology Service, Hospital Universitario de la Princesa, UAM, IIS-Princesa, Madrid, Spain.
Manuel IzquierdoInstituto de Investigaciones Biomédicas "Alberto Sols", Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid (CSIC-UAM), Madrid, Spain.
Noa B Martín-CófrecesImmunology Service, Instituto de Investigación Sanitaria del Hospital Universitario La Princesa (IIS-Princesa), Madrid, Spain.
Hospital Universitario de La Princesa · ESUniversidad Autónoma de Madrid · ESCentro de Investigación en Red en Enfermedades Cardiovasculares · ESSpanish National Centre for Cardiovascular Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The organization of the mitochondrial network is relevant for the metabolic fate of T cells and their ability to respond to TCR stimulation. This arrangement depends on cytoskeleton dynamics in response to TCR and CD28 activation, which allows the polarization of the mitochondria through their change in shape, and their movement along the microtubules towards the immune synapse. This work focus on the role of End-binding protein 1 (EB1), a protein that regulates tubulin polymerization and has been previously identified as a regulator of intracellular transport of CD3-enriched vesicles. EB1-interferred cells showed defective intracellular organization and metabolic strength in activated T cells, pointing to a relevant connection of the cytoskeleton and metabolism in response to TCR stimulation, which leads to increased AICD. By unifying the organization of the tubulin cytoskeleton and mitochondria during CD4

Indexed as

CD4-Positive T-LymphocytesMicrotubule-Associated ProteinsMitochondriaCD28 AntigensCytoskeletonHumansImmunological SynapsesJurkat CellsMembrane Potential, MitochondrialReceptors, Antigen, T-CellTubulinCD28 AntigensMAPRE1 protein, humanMicrotubule-Associated ProteinsReceptors, Antigen, T-CellTubulincell asymmetrycytoskeletonEB1glycolysismitochondriaT cell receptor

Identifiers

PMID37520527
PMCPMC10374013
OpenAlexW4384154627

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.