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To further verify these results, we perturbed mitochondria-ER appositions by treating activated EM CD8+ T cells with the ER stress blocker, 4-PBA, since reduction of ER stress has been shown to reduce mitochondria-ER interaction in non-immune cells (Prasad et al.,2016).
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Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8+ T Cells
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