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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...
The JAK-STAT Signaling Pathway01:20

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...
NF-kB-dependent Signaling Pathway02:26

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...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

Updated: Jun 17, 2026

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
08:52

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

DCLK1-dependent NF-κB activation mediates p-STAT3-induced osteoarthritis progression.

Pengfei Li1, Chipiu Wong2, Yuqiang Wang1

  • 1Department of Orthopedic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Clinical and Translational Medicine
|June 16, 2026
PubMed
Summary

This study reveals a new pathway involving phosphorylated STAT3 (p-STAT3) and DCLK1 that drives osteoarthritis (OA) progression. Targeting this p-STAT3/DCLK1 axis offers a potential therapeutic strategy for OA.

Keywords:
DCLK1NF‐κB pathwayextracellular matrix metabolismosteoarthritisphosphorylated STAT3

Related Experiment Videos

Last Updated: Jun 17, 2026

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
08:52

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathology

Background:

  • Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage destruction.
  • Signal transducer and activator of transcription 3 (STAT3) plays a key role in OA pathogenesis.
  • Downstream pathways of phosphorylated STAT3 (p-STAT3) in chondrocyte extracellular matrix (ECM) metabolism are not fully understood.

Purpose of the Study:

  • To identify novel p-STAT3-mediated pathways involved in OA.
  • To elucidate the role of p-STAT3 in regulating chondrocyte ECM metabolism.
  • To explore potential therapeutic targets for OA intervention.

Main Methods:

  • Detection of p-STAT3 expression in human and mouse OA cartilage.
  • Generation of chondrocyte-specific STAT3 knockout mice to assess OA progression.
  • RNA sequencing and CUT&Tag-seq to identify p-STAT3 downstream targets.
  • Molecular interaction and pathway validation assays.

Main Results:

  • P-STAT3 was significantly upregulated in OA cartilage.
  • STAT3 knockout attenuated OA progression.
  • P-STAT3 directly activated DCLK1 transcription.
  • DCLK1 promoted IKKβ phosphorylation and NF-κB activation, leading to increased MMP13 and decreased COL2A1 expression.

Conclusions:

  • A novel p-STAT3/DCLK1/IKKβ/NF-κB signaling axis regulates chondrocyte ECM metabolism and OA progression.
  • DCLK1 is a direct transcriptional target of p-STAT3.
  • The p-STAT3/DCLK1 axis represents a promising therapeutic target for OA.