2026-04-29T22:57:37Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/164042024-09-21T11:39:14Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Gómez-Morón, Álvaro
author
Requena, Silvia
author
Pertusa, Clara
author
Lozano-Prieto, Marta
author
Calzada-Fraile, Diego
author
Scagnetti, Camila
author
Sánchez-García, Inés
author
Calero-García, Ana Adela
author
Izquierdo, Manuel
author
Martín-Cófreces, Noa B
funder
Comunidad de Madrid (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Ministerio de Economía y Competitividad (España)
funder
Ministerio de Ciencia e Innovación (España)
funder
Instituto de Salud Carlos III
funder
Fundación La Caixa
funder
Ministerio de Ciencia e Innovación. Centro de Excelencia Severo Ochoa (España)
funder
Fundación ProCNIC
2023-09-05T08:14:05Z
2023-09-05T08:14:05Z
2023
Front Immunol. 2023 Jul 13;14:1197289.
10.3389/fimmu.2023.1197289
1664-3224
Frontiers in immunology
37520527
http://hdl.handle.net/20.500.12105/16404
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+ T cell activation, this work highlights the importance of this connection for critical cell asymmetry together with metabolic functions such as glycolysis, mitochondria respiration, and cell viability.
eng
End-binding protein 1 regulates the metabolic fate of CD4+ T lymphoblasts and Jurkat T cells and the organization of the mitochondrial network.
journal article
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End-binding protein 1 regulates_Front Immunol_2023.pdf
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End-binding protein 1 regulates_Front Immunol_2023.pdf.txt