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May 3, 2024iScienceOpen Access

Ablation of Atp5if1 impairs metabolic reprogramming and proliferation of T lymphocytes and compromises mouse survival

Inés Romero-Carramiñana Sonia Domínguez-Zorita Pau B. Esparza‐Moltó José M. Cuezva

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Abstract

T cells experience metabolic reprogramming to an enhanced glycolysis upon activation. Herein, we have investigated whether ATPase Inhibitory Factor 1 (IF1), the physiological inhibitor of mitochondrial ATP synthase, participates in rewiring T cells to a particular metabolic phenotype. We show that the activation of naive CD4

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Romero-Carramiñana et al. (2024) studied this question.

synapsesocial.com/papers/68e6ba6ab6db64358763ae34 https://doi.org/10.1016/j.isci.2024.109863

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Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1The ATPase Inhibitory Factor 1 (IF1) Contributes to the Warburg Effect and Is Regulated by Its Phosphorylation in S39 by a Protein Kinase A-like Activity2024 · 8 citations
2IF1 Promotes Cellular Proliferation and Inhibits Oxidative Phosphorylation in Mouse Embryonic Fibroblasts under Normoxia and Hypoxia2024 · 4 citations
3Upregulation of mitochondrial ATPase inhibitory factor 1 (ATPIF1) mediates increased glycolysis in mouse heartspreclinical · 2022 · 54 citations
4The critical role of Atpif1 in Her2-targeted CAR-T cell therapy for solid tumor via modulation of metabolism and mtDNA-STING signal pathwayOriginal Research · 2026
5ATP Synthase Inhibitory Factor-1 Deficiency Attenuates Doxorubicin Cardiotoxicity by Preserving Mitochondrial Structure and Functionpreclinical · 2026

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