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Identification of nucleolin and nucleophosmin as genotoxic stress-responsive RNA-binding proteins

Chonglin Yang1, Dony A Maiguel, France Carrier

  • 1University of Maryland, Baltimore, School of Medicine, Biochemistry and Molecular Biology Department, 108 North Greene Street, Baltimore, MD 21201-1503, USA.

Insights

Genotoxic stress activates RNA-binding proteins like nucleophosmin (NPM) and nucleolin in mammalian cells. This study identifies NPM and nucleolin as key players in the cellular response to DNA damage.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Genotoxic stress, or DNA damage, triggers complex cellular responses including signal transduction, gene activation, DNA repair, and apoptosis.
  • Previous research indicated that DNA-damaging agents can enhance the RNA-binding activity of specific proteins interacting with double stem-loop RNA structures.

Purpose of the Study:

  • To identify and characterize RNA-binding proteins that respond to genotoxic stress.
  • To elucidate the role of nucleophosmin (NPM) and nucleolin in cellular responses to DNA damage.

Main Methods:

  • Purification and identification of stress-responsive RNA-binding proteins.
  • Analysis of protein expression levels and RNA-binding activity following UV and ionizing radiation exposure.
  • Identification of mRNA targets regulated by nucleolin using RNA-binding assays.

Main Results:

  • Nucleophosmin (NPM) and nucleolin were identified as genotoxic stress-responsive RNA-binding proteins.
  • UV radiation increased NPM expression and RNA-binding activity; UV and ionizing radiation elevated nucleolin RNA-binding activity.
  • Nucleolin was found to potentially regulate 40 mRNA targets, including stress-responsive transcripts, with its activity mediated by p38 kinase.

Conclusions:

  • Nucleophosmin (NPM) and nucleolin are integral components of the mammalian cellular response to genotoxic stress.
  • The activation of RNA-binding capabilities by these proteins is a significant aspect of DNA damage response pathways.

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