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Related Concept Videos

Regulation of the Unfolded Protein Response01:31

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
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NLRX1 Regulation Following Acute Mitochondrial Injury.

Xiaogang Chu1, Songwei Wu2, Raghavan Raju1

  • 1Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, GA, United States.

Frontiers in Immunology
|November 19, 2019
PubMed
Summary
This summary is machine-generated.

NLRX1 protein helps maintain cellular balance after mitochondrial injury by regulating innate immunity. Its absence worsens immune responses and cell death, highlighting its protective role.

Keywords:
DAMPNLRX1PAMPinflammasomeinnate immunitymitochondriatrauma

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Area of Science:

  • Mitochondrial biology
  • Cellular energetics
  • Innate immunity

Background:

  • Mitochondrial dysfunction is linked to metabolic, cardiovascular, and neurological disorders.
  • NLRX1, a mitochondrial protein, modulates innate immunity and cell death.
  • The role of NLRX1 in cellular homeostasis post-mitochondrial injury remains unclear.

Purpose of the Study:

  • Investigate NLRX1's role in cellular homeostasis following acute mitochondrial injury.
  • Elucidate mechanisms of NLRX1 signaling pathway regulation under stress.

Main Methods:

  • Utilized an in vitro model of mitochondrial injury using rat pulmonary microvascular endothelial cells.
  • Induced injury via sodium azide treatment and glucose starvation.
  • Analyzed NF-κB and TBK1 activation, and protein recruitment to mitochondria.

Main Results:

  • Sodium azide and glucose starvation activated NF-κB and TBK1-mediated innate immune responses.
  • TBK1, IKK, IκB, and TRAF6 were recruited to mitochondria and interacted with NLRX1.
  • NLRX1 depletion exacerbated immune responses and apoptosis.

Conclusions:

  • NLRX1 regulates mitochondrial innate immune responses.
  • NLRX1 is crucial for maintaining cellular homeostasis after acute mitochondrial injury.
  • Mitochondrial recruitment of inflammatory mediators and NLRX1 interaction are protective.