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S100A7 in Psoriasis: Immunodetection and Activation by CRISPR technology

  • Mariagrazia Granata
  • Evangelia Skarmoutsou
  • Maria Clorinda Mazzarino
  • Fabio D’AmicoEmail author
Protocol
Part of the Methods in Molecular Biology book series (MIMB, volume 1929)

Abstract

Psoriasis, an inflammatory autoimmune skin disease, is the result of a chronic interaction between hyperproliferative keratinocytes and infiltrating activated immune cells. The mechanisms underlying psoriasis pathogenesis remain largely unknown, although a combination of genetic and environmental factors plays an important role in its development. S100A7 is overexpressed in psoriasis, and there is growing evidence that S100A7 may be involved in the pathogenesis of psoriasis. Since the mechanisms underlying S100A7 regulation and function remain elusive, a better understanding of these mechanisms may be useful to uncover additional treatment approaches for psoriasis. Immunohistology provides invaluable tools for a better understanding of the pathogenetic mechanisms of psoriasis. Here, we describe basic methods for immunofluorescence and immunohistochemistry analysis of S100A7 expression in psoriatic patients as well as in S100A7 CRISPR-activated human keratinocyte cell line.

Key words

S100A7 Psoriasis Calcium EF-hand CRISPR Immunofluorescence Immunohistochemistry 

Notes

Acknowledgment

This work was supported by intramural grants from the University of Catania, Italy.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Mariagrazia Granata
    • 1
  • Evangelia Skarmoutsou
    • 1
  • Maria Clorinda Mazzarino
    • 1
  • Fabio D’Amico
    • 1
    Email author
  1. 1.Department of Biomedical and Biotechnological SciencesUniversity of CataniaCataniaItaly

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