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NF-kB-dependent Signaling Pathway

NF-kB-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...

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
The heterodimer of NF-κB...

The JAK-STAT Signaling Pathway

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...

Non-Canonical Wnt Signaling Pathways

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Non-Canonical Wnt Signaling Pathways

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Related Experiment Video

Updated: Jun 15, 2026

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

Published on: January 27, 2023

NF-kappaB signaling: multiple angles to target OA.

Kenneth B Marcu¹, Miguel Otero, Eleonora Olivotto

¹Biochemistry and Cell Biology Department, Stony Brook University, Stony Brook, NY 11794, USA. kenneth.marcu@stonybrook.edu

Current Drug Targets

|March 5, 2010

Summary

This summary is machine-generated.

Nuclear factor-kappa B (NF-kappaB) signaling plays a dual role in osteoarthritis (OA) by driving inflammation and promoting chondrocyte differentiation. Targeting NF-kappaB activating kinases offers a promising therapeutic strategy for OA.

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Last Updated: Jun 15, 2026

Creation of a Knee Joint-on-a-Chip for Modeling Joint Diseases and Testing Drugs

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Published on: January 27, 2023

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

Area of Science:

Biochemistry
Molecular Biology
Rheumatology

Background:

Osteoarthritis (OA) pathogenesis involves inflammation and chondrocyte dysregulation.
Nuclear factor-kappa B (NF-kappaB) signaling is activated by various OA-related stressors.
NF-kappaB influences inflammatory mediators and chondrocyte differentiation.

Purpose of the Study:

To investigate the multifaceted role of NF-kappaB signaling in OA.
To identify NF-kappaB activating kinases as potential therapeutic targets for OA.

Main Methods:

Review of existing literature on NF-kappaB signaling in OA.
Analysis of NF-kappaB's influence on chondrocyte differentiation and extracellular matrix (ECM) remodeling.
Discussion of targeted therapeutic strategies against NF-kappaB pathways.

Main Results:

NF-kappaB activation contributes to OA inflammation and aberrant chondrocyte hypertrophy.
NF-kappaB signaling impacts ECM components and chondrocyte maturation regulators like beta-catenin and Runx2.
NF-kappaB activating kinases (IKKalpha, IKKbeta) are identified as key targets.

Conclusions:

NF-kappaB signaling is a critical mediator in OA, affecting both inflammation and chondrocyte fate.
Targeted inhibition of NF-kappaB kinases presents a novel therapeutic avenue for OA.
Further in vivo studies are needed to evaluate specific inhibitors and localized delivery for OA treatment.