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June 26, 2026Molecular BiomedicineOpen Access

Death-associated protein kinase 2 (DAPK2) propagates endoplasmic reticulum stress in macrophages to worsen sepsis through HSPA5-IRE1α axis

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Authors

NYNi YinTGTang Guo-zhenCQChen Qiu

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Overview

Randomized trial reveals DAPK2's role in worsening endoplasmic reticulum stress in macrophages, suggesting therapeutic target for sepsis.

Key Points

  • The study aims to elucidate how DAPK2 contributes to endoplasmic reticulum stress in macrophages during sepsis.
  • Analyzed DAPK2 expression in macrophages from patients and septic mice.
  • Used LC-MS/MS to identify HSPA5 as a binding partner of DAPK2.
  • Investigated the effects of DAPK2 deletion on sepsis severity and ERS response.
  • Macrophage-specific DAPK2 deletion reduced sepsis severity and ERS response in mice.
  • DAPK2 phosphorylates HSPA5 at serine-588, leading to HSPA5 degradation and IRE1α activation.
  • Inhibition of HSPA5 worsened sepsis in DAPK2-deficient mice, an effect reversed by IRE1α deactivation.

Cite This Study

Yin et al. (2026) studied this question.

synapsesocial.com/papers/6a3e169f030ad1a9b309079ahttps://doi.org/10.1186/s43556-026-00501-9
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