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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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MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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
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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Transducer Mechanism: Nuclear Receptors01:31

Transducer Mechanism: Nuclear Receptors

Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
About 48 different soluble family members of nuclear receptors are identified that can be divided into two main classes:
Co-activators and Co-repressors02:04

Co-activators and Co-repressors

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...

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Updated: Jun 9, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/&#945;
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A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

The RET/PTC3 oncogene activates classical NF-κB by stabilizing NIK.

R J Neely1, M S Brose, C M Gray

  • 1Department of Animal Biology, University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, USA.

Oncogene
|September 7, 2010
PubMed
Summary
This summary is machine-generated.

The RET/PTC3 fusion protein activates nuclear factor-kappa B (NF-κB) signaling in thyroid cancer by stabilizing NF-κB-inducing kinase (NIK). This discovery reveals a new oncogene-driven mechanism for NF-κB activation.

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NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
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NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • The RET/PTC3 (RP3) fusion protein, found in papillary thyroid carcinoma (PTC), activates nuclear factor-kappa B (NF-κB) and pro-inflammatory gene expression.
  • The precise mechanism by which RP3 activates NF-κB remains unclear.

Purpose of the Study:

  • To elucidate the mechanism of RP3-mediated NF-κB activation.
  • To investigate the role of NF-κB signaling components in RP3-induced inflammation.

Main Methods:

  • RP3 was expressed in murine embryonic fibroblasts (MEFs) deficient in key NF-κB signaling molecules.
  • NF-κB activation, gene expression, and protein levels (NIK, TRAF3) were analyzed.
  • Inhibition studies using a NEMO-binding peptide and dominant-negative NIK were performed.
  • PTC specimens were examined for NIK expression.

Main Results:

  • RP3 upregulated pro-inflammatory genes (CCL2, CXCL1, GM-CSF, TNF) and activated classical NF-κB in wild-type MEFs.
  • Activation occurred in IKKβ(-/-) MEFs but not in IKKα- or NEMO-deficient cells.
  • RP3 increased NIK levels and failed to activate NF-κB in NIK-deficient MEFs.
  • RP3-induced NF-κB activation was blocked by dominant-negative NIK and required NEMO and IKKα.
  • NIK stabilization by RP3 occurred independently of TRAF3 degradation.
  • PTC samples showed strong NIK staining.

Conclusions:

  • RP3 activates classical NF-κB through a pathway involving NIK, NEMO, and IKKα.
  • This study reveals a novel mechanism of oncogene-induced NF-κB activation mediated by NIK stabilization.