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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.
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
NF-kB-dependent Signaling Pathway02:26

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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.
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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...
Tooth Anatomy01:21

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Related Experiment Video

Updated: Jul 14, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Nuclear factor kappaB p65 phosphorylation in orthodontic tooth movement.

J Zuo1, L A Archer, A Cooper

  • 1Department of Orthodontics, 1600 SW Archer Road, Campus Box 100444, University of Florida College of Dentistry, Gainesville, FL 32610, USA.

Journal of Dental Research
|May 26, 2007
PubMed
Summary

Phosphorylation of nuclear factor kappaB (NFkappaB) at p65*(536) rapidly increases with orthodontic tooth movement. This suggests p65*(536) plays a key role in bone remodeling during orthodontic treatment.

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Last Updated: Jul 14, 2026

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
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Published on: April 1, 2022

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09:33

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The Establishment of a Murine Maxillary Orthodontic Model
04:11

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Published on: October 27, 2023

Area of Science:

  • Biomedical Science
  • Orthodontics
  • Cell Biology

Background:

  • Osteoclasts are crucial for orthodontic tooth movement.
  • Nuclear factor kappaB (NFkappaB) transactivation, specifically p65*(536) phosphorylation, is implicated in osteoclast differentiation via receptor activator of nuclear factor kappaB-ligand (RANK-L).

Purpose of the Study:

  • To investigate the role of p65*(536) in alveolar bone cell responses during orthodontic tooth movement.
  • To determine if the NFkappaB transactivation pathway is involved in the cellular mechanisms of orthodontic treatment.

Main Methods:

  • Assessing p65*(536) levels in rat alveolar bone cells following orthodontic stimuli.
  • Examining p65*(536) expression in osteoclast-like cells in response to RANK-L and mechanical scraping in vitro.

Main Results:

  • A significant surge in p65*(536) levels was observed 3 and 12 hours post-orthodontic stimulation in rats.
  • Osteoclast-like cells showed no change in p65*(536) with RANK-L but a rapid increase upon mechanical scraping.

Conclusions:

  • p65*(536) is quickly generated in response to orthodontic stimuli and mechanical stress.
  • The p65*(536) pathway is likely a significant factor in the bone remodeling processes that occur during orthodontic tooth movement.