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Related Experiment Video

Updated: Feb 12, 2026

Preparation of Keratin Hydrolysate from Chicken Feathers and Its Application in Cosmetics
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Keratins Regulate p38MAPK-Dependent Desmoglein Binding Properties in Pemphigus.

Franziska Vielmuth1, Elias Walter1, Michael Fuchs1

  • 1Faculty of Medicine, Institute of Anatomy, Ludwig-Maximilians-Universität München, Munich, Germany.

Frontiers in Immunology
|April 5, 2018
PubMed
Summary

Keratins are crucial for cell adhesion in pemphigus. Autoantibodies disrupt keratin organization, but p38MAPK signaling, regulated by keratins, is key to adhesion loss, affecting both keratin-dependent and -independent pathways.

Keywords:
atomic force microscopydesmogleindesmosomekeratinp38MAPK

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Area of Science:

  • Cell Biology
  • Dermatology
  • Immunology

Background:

  • Keratins are vital for desmosome anchorage.
  • Pemphigus vulgaris and foliaceus involve autoantibodies against desmogleins (Dsg1/3), causing keratin disorganization and cell adhesion loss.
  • The precise role of keratin organization in autoantibody-induced adhesion loss remains unclear.

Purpose of the Study:

  • To investigate the significance of keratin organization in pemphigus pathogenesis.
  • To dissect the role of keratins in autoantibody-mediated loss of intercellular adhesion.
  • To elucidate the involvement of p38MAPK signaling in pemphigus adhesion disruption.

Main Methods:

  • Utilized wild-type (wt) and keratin-deficient (KtyII k.o.) murine keratinocytes.
  • Applied pemphigus autoantibodies and anisomycin (p38MAPK activator).
  • Analyzed intercellular adhesion, desmoglein interactions (atomic force microscopy), and p38MAPK activation.

Main Results:

  • Keratin-deficient cells exhibited reduced adhesion, not further impaired by pemphigus autoantibodies.
  • Pemphigus autoantibodies induced keratin retraction in wt cells but not KtyII k.o. cells.
  • p38MAPK activation was critical for adhesion loss in wt cells and partially restored adhesion in KtyII k.o. cells.

Conclusions:

  • Keratins are not essential for direct desmoglein interaction inhibition by autoantibodies.
  • p38MAPK signaling plays a critical role in regulating cell adhesion, influenced by keratin presence.
  • Keratin-dependent and -independent mechanisms mediated by p38MAPK contribute to pemphigus pathogenesis.