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Related Concept Videos

Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

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Related Experiment Video

Updated: May 19, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

PKR stirs up inflammasomes.

H James Stunden1, Eicke Latz

  • 1Institute of Innate Immunity, Biomedical Center, University Hospitals Bonn, Sigmund-Freud-Str. 25, Bonn 53127, Germany.

Cell Research
|September 5, 2012
PubMed
Summary
This summary is machine-generated.

Protein Kinase R (PKR) activates multiple inflammasomes, including NLRP1, NLRP3, NLRC4, and AIM2. This discovery offers a new therapeutic target for treating diseases linked to inflammasome overactivation.

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Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
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Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

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Last Updated: May 19, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

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Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages
08:41

Visualization of Inflammatory Caspases Induced Proximity in Human Monocyte-Derived Macrophages

Published on: April 6, 2022

Area of Science:

  • Immunology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Inflammasomes are critical immune sensors that activate caspase-1, maturing pro-inflammatory cytokines like IL-1β.
  • The precise upstream activators of inflammasomes, especially NLRP3, are not fully elucidated.
  • Dysregulated inflammasome activity contributes to various inflammatory diseases.

Purpose of the Study:

  • To investigate the upstream mechanisms of inflammasome activation.
  • To identify novel regulators of inflammasome assembly and function.
  • To explore potential therapeutic targets for inflammasome-mediated pathologies.

Main Methods:

  • Utilized cell-based assays to study inflammasome activation pathways.
  • Investigated the role of Protein Kinase R (PKR) in inflammasome complex formation.
  • Assessed the activation of various inflammasome sensors (NLRP1, NLRP3, NLRC4, AIM2) in response to PKR activity.

Main Results:

  • Identified a previously unrecognized role for Protein Kinase R (PKR) in inflammasome activation.
  • Demonstrated that PKR can activate multiple inflammasome complexes, including NLRP1, NLRP3, NLRC4, and AIM2.
  • PKR-mediated inflammasome activation leads to caspase-1 maturation and subsequent cytokine processing.

Conclusions:

  • Protein Kinase R (PKR) is a novel upstream activator of key inflammasome complexes.
  • Targeting PKR may offer a new therapeutic strategy for managing inflammasome-driven inflammatory conditions.
  • Further research into PKR's role can elucidate complex inflammatory signaling networks.