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Cells from patients with ataxia telangiectasia (AT) build up too much glycogen because of faulty glucose metabolism and weak mitochondrial respiration. The study shows that blocking a protein called FNIP2 can partially fix these metabolic problems by boosting calcium signaling and mitochondrial activity, improving cell survival and suggesting a new possible treatment target for AT.

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This page is a summary of: Targeting the FNIP2-SERCA2b axis improves metabolic and mitochondrial defects in Ataxia Telangiectasia, Cell Death and Disease, March 2026, Springer Science + Business Media,
DOI: 10.1038/s41419-026-08507-5.
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