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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...
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...
MAPK Signaling Cascades01:07

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...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Related Experiment Video

Updated: Jun 22, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Nrf2 signaling and cell survival.

Suryakant K Niture1, James W Kaspar, Jun Shen

  • 1Department of Pharmacology, University of Maryland School of Medicine, 655 West Baltimore Street, Baltimore, MD 21201, USA.

Toxicology and Applied Pharmacology
|June 23, 2009
PubMed
Summary

The Nrf2 (Nuclear factor erythroid 2-related factor 2) and INrf2 (inhibitor of Nrf2) proteins form an auto-regulatory loop. This loop controls cellular defense genes, protecting cells from oxidative stress and promoting survival.

Related Experiment Videos

Last Updated: Jun 22, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Area of Science:

  • Cellular biology
  • Molecular mechanisms of stress response

Background:

  • Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating cellular defense against oxidative and electrophilic stress.
  • The inhibitor of Nrf2 (INrf2) protein targets Nrf2 for degradation under basal conditions, acting as a crucial regulator of Nrf2 stability and activity.

Purpose of the Study:

  • To elucidate the intricate regulatory mechanisms governing Nrf2 activity and its interaction with INrf2.
  • To understand how oxidative and electrophilic stress signals modulate Nrf2 localization and degradation.
  • To investigate the auto-regulatory feedback loop between Nrf2 and INrf2.

Main Methods:

  • The study likely involved molecular biology techniques to investigate protein-protein interactions, cellular localization, and gene expression.
  • Analysis of post-translational modifications (phosphorylation, ubiquitination) of Nrf2 and INrf2.
  • Investigating the role of specific signaling pathways (PKC, GSK-3beta) and proteins (Fyn, Prothymosin-alpha) in Nrf2 regulation.

Main Results:

  • Under stress, Nrf2 dissociates from INrf2, translocates to the nucleus, and activates protective genes via the antioxidant response element (ARE).
  • Specific modifications (e.g., INrf2 Cys151, Nrf2 Ser40 phosphorylation) facilitate Nrf2 release and nuclear entry.
  • A delayed stress response involves GSK-3beta and Fyn, leading to Nrf2 phosphorylation, nuclear export, and degradation, alongside INrf2-mediated nuclear degradation.
  • An auto-regulatory loop exists where Nrf2 controls INrf2 transcription, and INrf2 degrades Nrf2 in both cellular compartments.

Conclusions:

  • The dynamic interplay between Nrf2 and INrf2, involving stress-induced modifications and degradation pathways, precisely controls Nrf2 levels and target gene activation.
  • This auto-regulatory mechanism ensures rapid adaptation to oxidative/electrophilic stress and promotes cell survival.
  • Fine-tuning of Nrf2 activity is critical for cellular defense and maintaining homeostasis.