TECR palmitoylation triggers a necrotic cell death program driving acute liver injury.

Multi-site palmitoylation of ER-resident TECR activates PERK-dependent ER stress signaling to trigger TECR-dependent necrotic cell death in mouse models of acute liver injury.

• Why it matters: Acute liver injury from drug toxicity or immune activation has limited mechanistic clarity and few effective therapies, motivating identification of specific regulated death pathways.
• What they did: The study mapped TECR palmitoylation control by ZDHHC5 and ZDHHC2 and reversal by ABHD10, then tested PERK-dependent ER stress and necrotic death in acetaminophen- and concanavalin A-induced hepatotoxicity models.
• The result: TPNCD contributes to liver injury in these mouse models and is reduced by hepatocyte-specific TECR ablation or pharmacological inhibition of palmitoylation or ER stress signaling, suggesting therapeutic entry points.

AI summary of the abstract · may contain errors · not medical advice · read the paper.