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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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Related Experiment Video

Updated: Nov 10, 2025

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

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Published on: March 24, 2017

Isoform-Selective NFAT Inhibitor: Potential Usefulness and Development.

Noriko Kitamura¹, Osamu Kaminuma^1,2

¹Laboratory of Allergy and Immunology, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.

International Journal of Molecular Sciences

|April 3, 2021

Summary

Nuclear factor of activated T cells (NFAT) are crucial in immunity and disease. Targeting specific NFAT isoforms offers a novel therapeutic strategy to improve drug efficacy and reduce side effects associated with current broad-spectrum immunosuppressants.

Keywords:

aortic smooth muscle cell calcineurin-binding region cytokine immunoprecipitation immunosuppressant knockout mouse molecular operating environment nuclear localization signal

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Last Updated: Nov 10, 2025

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Published on: March 24, 2017

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A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

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Published on: December 4, 2018

Area of Science:

Immunology
Molecular Biology
Pharmacology

Background:

Nuclear factor of activated T cells (NFAT) are key regulators in T cells and other biological processes.
Dysfunctional NFAT is implicated in the pathogenesis of various organ-specific diseases.
The NFAT family comprises five isoforms with distinct functions and expression patterns.

Purpose of the Study:

To review the roles of NFAT family members in biological events and disease development.
To analyze the efficacy and limitations of current NFAT-targeting therapies, including immunosuppressants like cyclosporine and tacrolimus.
To explore the potential of isoform-selective NFAT regulation for developing improved therapeutics.

Main Methods:

Literature review of NFAT functions, disease associations, and therapeutic strategies.
Analysis of structural differences among NFAT isoforms.
Evaluation of current immunosuppressants targeting NFAT activity.

Main Results:

NFAT proteins are involved in diverse biological functions and disease pathogenesis.
Current broad-acting immunosuppressants targeting NFAT cause significant side effects due to inhibiting multiple isoforms.
Isoform-selective targeting of NFAT remains largely unexplored but holds therapeutic promise.

Conclusions:

Targeting specific NFAT isoforms could overcome the limitations of current broad-spectrum immunosuppressants.
Developing drugs that selectively regulate NFAT isoforms may lead to more effective and safer therapies.
Further research into molecular mechanisms for isoform-selective NFAT regulation is warranted.