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

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

9.1K
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...
9.1K
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

2.4K
Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
2.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

6.7K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.7K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.8K
The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
3.8K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

2.5K
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...
2.5K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

6.5K
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...
6.5K

You might also read

Related Articles

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

Sort by
Same author

Homeostatic mature dendritic cells instruct fibroblast specialization via Notch2 signaling to establish T cell niches.

Immunity·2026
Same author

Interferon-γ causes myogenic cell dysfunction and senescence in immune myopathies.

Brain : a journal of neurology·2025
Same author

Dysregulation of inflammasomes in autoinflammatory diseases.

Joint bone spine·2025
Same author

The integrin CD11b inhibits MSU-induced NLRP3 inflammasome activation in macrophages and protects mice against MSU-induced joint inflammation.

Arthritis research & therapy·2024
Same author

HSP90β controls NLRP3 autoactivation.

Science advances·2024
Same author

Receptor interacting protein kinase-3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy.

Journal of cachexia, sarcopenia and muscle·2023
Same journal

Single-nucleotide RNA m<sup>6</sup>A mapping in bovine preimplantation development reveals site-specific regulation of RPL12 at zygotic genome activation.

Cell reports·2026
Same journal

M4-ipRGCs regulate contrast sensitivity in vision.

Cell reports·2026
Same journal

Plasmodium falciparum HSP90 inhibitors show divergent resistance despite a shared ATP-binding site.

Cell reports·2026
Same journal

Structural proteomics reveals that misfolded nascent proteins expose buried lysines for ubiquitination and rapid proteasomal degradation.

Cell reports·2026
Same journal

Physical interactions within the SIR heterochromatin complex potentiate inter-subunit communication and gene repression.

Cell reports·2026
Same journal

An IGF2BP3-dependent metabolic circuit governs macrophage recruitment and immunosuppression in glioblastoma.

Cell reports·2026
See all related articles

Related Experiment Video

Updated: Aug 21, 2025

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

10.8K

CDC42 regulates PYRIN inflammasome assembly.

Lotte Spel1, Lea Zaffalon1, Cyrielle Hou1

  • 1Department of Immunobiology, University of Lausanne, 155 Ch. des Boveresses, 1066 Epalinges, Switzerland.

Cell Reports
|November 17, 2022
PubMed
Summary
This summary is machine-generated.

The PYRIN inflammasome pathway, crucial for immunity, can cause autoinflammation when overactive. This study identifies CDC42 as essential for PYRIN inflammasome assembly and function in autoinflammatory diseases.

Keywords:
CDC42CP: ImmunologyFMFMEFVNOCARHPAANDPYRINRhoAinflammasomesmall GTPase

More Related Videos

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

3.3K
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1&#946; 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

21.0K

Related Experiment Videos

Last Updated: Aug 21, 2025

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

10.8K
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

3.3K
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1&#946; 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

21.0K

Area of Science:

  • Immunology
  • Cell Biology
  • Genetics

Background:

  • The PYRIN inflammasome is integral to innate immunity against pathogens.
  • Dysregulated PYRIN inflammasome activation causes autoinflammation, exemplified by familial Mediterranean fever (FMF).
  • Molecular mechanisms governing PYRIN inflammasome assembly, including dephosphorylation and oligomerization, remain unclear.

Purpose of the Study:

  • To identify novel regulators of PYRIN inflammasome function using a functional genetics approach.
  • To elucidate the role of the small Rho GTPase CDC42 in PYRIN inflammasome activation and assembly.

Main Methods:

  • Functional genetics screen to identify PYRIN inflammasome regulators.
  • Analysis of CDC42's impact on PYRIN activity, phosphorylation, and inflammasome complex oligomerization.

Main Results:

  • CDC42 was identified as essential for PYRIN inflammasome activity and oligomerization.
  • CDC42's catalytic activity inhibits PYRIN via phosphorylation, but its inflammasome-supportive role is independent of GDP/GTP binding.
  • CDC42's function in inflammasome assembly does not involve PYRIN dephosphorylation.

Conclusions:

  • CDC42 plays a dual role in regulating PYRIN inflammasome pathway.
  • CDC42 is a critical component required for PYRIN inflammasome assembly in both physiological and pathological conditions.
  • These findings offer new insights into the molecular basis of autoinflammatory diseases driven by PYRIN inflammasome dysregulation.