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iCLIP - Transcriptome-wide Mapping of Protein-RNA Interactions with Individual Nucleotide Resolution
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Published on: April 30, 2011

Expression and functional studies on the noncoding RNA, PRINS.

Krisztina Szegedi1, Anikó Göblös, Sarolta Bacsa

  • 1Department of Dermatology and Allergology, University of Szeged, Korányi fasor 6, H-6720 Szeged, Hungary. goblos.aniko@med.u-szeged.hu.

International Journal of Molecular Sciences
|January 25, 2013
PubMed
Summary
This summary is machine-generated.

This study reveals that PRINS, a noncoding RNA, interacts with nucleophosmin (NPM) and influences its cellular stress response in skin keratinocytes, potentially impacting psoriasis.

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10:34

Detection of RNA-binding Proteins by In Vitro RNA Pull-down in Adipocyte Culture

Published on: July 22, 2016

Area of Science:

  • Molecular Biology
  • Dermatology
  • RNA Biology

Background:

  • PRINS (Psoriasis susceptibility-related noncoding RNA) is implicated in psoriasis and cellular stress.
  • The cellular distribution and function of PRINS require further elucidation.

Purpose of the Study:

  • To investigate the cellular and histological distribution of PRINS.
  • To identify the protein interactors of PRINS and determine its role in cellular stress response.

Main Methods:

  • In situ hybridization for PRINS distribution.
  • Co-immunoprecipitation and Western blotting to identify PRINS interactors.
  • Immunohistochemistry to assess protein expression in skin samples.
  • UV-B irradiation and gene silencing experiments in keratinocytes.

Main Results:

  • PRINS shows variable expression in human tissues, with consistent patterns in epidermal keratinocytes.
  • Nucleophosmin (NPM) was identified as a physical interactor of PRINS.
  • NPM translocates within the nucleus upon UV-B irradiation in keratinocytes.
  • Silencing PRINS prevents NPM translocation in UV-B-irradiated keratinocytes.

Conclusions:

  • PRINS interacts with NPM and plays a role in the NPM-mediated cellular stress response in skin keratinocytes.
  • These findings suggest a novel mechanism involving PRINS in skin homeostasis and potentially in psoriasis pathogenesis.