Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
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 Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

NOD2 drives regenerative fetal-like reprogramming in the intestinal epithelium.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Host response to bacteria induces a shift towards the enteroendocrine cell lineage in the murine enteroid model.

PLoS pathogens·2026
Same author

New Perspectives on Paracrine IL-18 Signaling in the Intestinal Epithelium.

DNA and cell biology·2025
Same author

Bacterial ADP-heptose triggers stem cell regeneration in the intestinal epithelium following injury.

Cell stem cell·2025
Same author

The IL-18 receptor is expressed on murine small-intestinal enterochromaffin cells and executes a recovery program upon injury.

Proceedings of the National Academy of Sciences of the United States of America·2025
Same author

Lymph node macrophages drive immune tolerance and resistance to cancer therapy by induction of the immune-regulatory cytokine IL-33.

Cancer cell·2025

Related Experiment Video

Updated: Jun 22, 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

Knocking in the NLRP3 inflammasome.

Stephen E Girardin1

  • 1Department of Laboratory Medicine and Pathobiology, Medical Sciences Building, University of Toronto, Toronto, Ontario, Canada. stephen.girardin@utoronto.ca

Immunity
|June 23, 2009
PubMed
Summary

Researchers characterized Nlrp3 gene-targeted mice with mutations similar to those causing human autoinflammatory syndromes. This study provides a valuable model for investigating NLRP3-associated diseases.

Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Mutations in the human NLRP3 gene are linked to autoinflammatory syndromes, specifically those involving interleukin-1beta.
  • Understanding the function of NLRP3 is crucial for developing treatments for these conditions.

Purpose of the Study:

  • To characterize Nlrp3 gene-targeted mice that carry mutations mirroring those found in human NLRP3-associated autoinflammatory diseases.
  • To establish a preclinical model for studying the pathogenesis and potential therapies of these syndromes.

Main Methods:

  • Generation of Nlrp3 gene-targeted mouse models.
  • Phenotypic analysis of the generated mouse models.
  • Assessment of inflammasome activation and cytokine production.

More Related Videos

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

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

Published on: May 22, 2014

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Related Experiment Videos

Last Updated: Jun 22, 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
09:04

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

Published on: May 22, 2014

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Main Results:

  • The characterized Nlrp3 gene-targeted mice successfully mimic human disease-causing mutations.
  • These mouse models exhibit key features of autoinflammatory syndromes.
  • Analysis revealed altered inflammasome activity and cytokine profiles.

Conclusions:

  • Nlrp3 gene-targeted mice provide a robust preclinical model for studying human autoinflammatory diseases.
  • This research facilitates further investigation into NLRP3 inflammasome function and therapeutic strategies.