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NF-κB-dependent Signaling Pathway

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

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

Published on: May 22, 2014

Covalent Targeting As a Common Mechanism for Inhibiting NLRP3 Inflammasome Assembly.

Caroline Stanton^1,2, Jie Sun², Kayla Nutsch¹

¹Department of Chemistry, The Scripps Research Institute, La Jolla, California 92037, United States.

ACS Chemical Biology

|January 10, 2024

Summary

Researchers identified novel covalent compounds that inhibit the NLRP3 inflammasome, a key driver of inflammation. Targeting reactive cysteines on NLRP3 offers a promising strategy for treating inflammatory disorders.

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Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Area of Science:

Immunology
Molecular Biology
Drug Discovery

Background:

The NLRP3 inflammasome is crucial for inflammatory cytokine release (e.g., IL-1β, IL-18).
Dysregulated NLRP3 activation is linked to various inflammatory diseases.
Understanding NLRP3 regulation is vital for developing targeted therapies.

Purpose of the Study:

To identify novel inhibitors of NLRP3 inflammasome assembly and activity.
To explore covalent targeting of reactive cysteines within NLRP3.

Main Methods:

Development and implementation of a high-throughput screening assay.
Profiling of 20 new covalent compounds and known inhibitors.
Characterization of compound VLX1570's mechanism of action.

Main Results:

Identification of 20 novel covalent NLRP3 inhibitors across nine chemical scaffolds.
Demonstration that covalent targeting of NLRP3 cysteines inhibits inflammasome activation.
VLX1570 induces covalent, intermolecular cross-linking of NLRP3 cysteines.

Conclusions:

NLRP3 contains multiple reactive cysteines amenable to covalent inhibition.
Covalent compounds targeting NLRP3 cysteines represent a viable therapeutic strategy for inflammatory conditions.
Further development of electrophilic inhibitors for NLRP3 is warranted.