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S100A7, Jab1, and p27

Mariagrazia Granata1, Evangelia Skarmoutsou1, Pietro Gangemi2

  • 1Department of Biomedical and Biotechnological Sciences, University of Catania, Catania, Italy.

Journal of Cellular Biochemistry
|September 12, 2018
PubMed
Summary
This summary is machine-generated.

Psoriasis involves skin cell overgrowth. This study shows S100A7 protein interacts with Jab1, leading to reduced p27 Kip1 levels and contributing to impaired skin cell proliferation in psoriasis.

Keywords:
CRISPRCSN5S100A7c-jun activation domain-binding protein-1 (Jab1)keratinocytep27Kip1psoriasinpsoriasis

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Area of Science:

  • Dermatology
  • Cell Biology
  • Molecular Biology

Background:

  • Psoriasis is a chronic inflammatory skin disease marked by keratinocyte hyperproliferation.
  • S100A7, an EF-hand calcium-binding protein, is overexpressed in psoriatic skin.
  • Jab1, a c-Jun stabilizing cofactor, downregulates the cell cycle inhibitor p27 Kip1 in cancer models.

Purpose of the Study:

  • To investigate the interaction between S100A7 and Jab1.
  • To determine the downstream effects on p27 Kip1 expression in psoriasis.

Main Methods:

  • Utilized normal human keratinocytes transfected with S100A7 CRISPR activation plasmid.
  • Analyzed archival psoriatic skin samples.
  • Examined protein localization and expression patterns of S100A7, Jab1, and p27 Kip1.

Main Results:

  • Upregulated S100A7 colocalized with Jab1 in the nucleus of transfected cells and psoriatic samples.
  • Observed differential expression of Jab1 between cytoplasmic and nuclear compartments, suggesting translocation.
  • p27 Kip1 protein showed nuclear translocation and subsequent degradation patterns.

Conclusions:

  • S100A7 interacts with Jab1 at the nuclear level in psoriatic skin.
  • Jab1 translocation and subsequent p27 Kip1 degradation contribute to impaired keratinocyte proliferation in psoriasis.
  • This S100A7-Jab1-p27 Kip1 axis offers potential therapeutic targets for psoriasis.