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Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Nucleotide Excision Repair

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NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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NF-κB-dependent Signaling Mechanism
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Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

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Transducer Mechanism: Nuclear Receptors01:31

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NF-kB-dependent Signaling Pathway02:26

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Related Experiment Video

Updated: May 24, 2026

In Vivo Imaging of Reactive Oxygen Species in a Murine Wound Model
06:40

In Vivo Imaging of Reactive Oxygen Species in a Murine Wound Model

Published on: November 17, 2018

Nrf2 links epidermal barrier function with antioxidant defense.

Matthias Schäfer1, Hany Farwanah, Ann-Helen Willrodt

  • 1Department of Biology, Institute of Cell Biology, ETH Zurich, Zurich, Switzerland. matthias.schaefer@cell.biol.ethz.ch

EMBO Molecular Medicine
|March 3, 2012
PubMed
Summary

Activating the Nrf2 pathway in skin cells surprisingly caused epidermal thickening and inflammation. While enhancing protective proteins, it disrupted skin barrier function, impacting its use in treatments.

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Last Updated: May 24, 2026

In Vivo Imaging of Reactive Oxygen Species in a Murine Wound Model
06:40

In Vivo Imaging of Reactive Oxygen Species in a Murine Wound Model

Published on: November 17, 2018

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cell Biology

Background:

  • The skin's primary functions include barrier protection against environmental stressors and microbial invasion.
  • The transcription factor Nrf2 (Nuclear factor erythroid 2-related factor 2) is a key regulator of cellular defense mechanisms.

Purpose of the Study:

  • To investigate the role of Nrf2 activation in keratinocytes under stress conditions.
  • To determine the consequences of enhanced Nrf2 activity on skin barrier function and cellular processes.

Main Methods:

  • Pharmacological and genetic activation of Nrf2 in mouse keratinocytes.
  • Analysis of epidermal morphology, protein expression (Sprr 2d, 2h, Slpi), and cellular functions (desquamation, proliferation).

Main Results:

  • Enhanced Nrf2 activity led to epidermal thickening, hyperkeratosis, and inflammation, mimicking lamellar ichthyosis.
  • Upregulation of small proline-rich proteins (Sprrs) and secretory leukocyte peptidase inhibitor (Slpi) were identified as novel Nrf2 targets.
  • Impaired desquamation, altered lipid barrier, and keratinocyte hyperproliferation were observed, alongside corneocyte fragility.

Conclusions:

  • Nrf2 activation in keratinocytes has a dual role: it enhances protective protein expression but also disrupts skin barrier integrity.
  • The findings reveal an unexpected role for Nrf2 in epidermal homeostasis and highlight potential risks for pharmacological Nrf2 activation in skin conditions.