Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of

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Updated: Jun 14, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Gudrun Ziegeler1, Jie Ming2, Jana C Koseki1

  • 1Harvard Medical School, Boston, Massachusetts 02115.

The Journal of Biological Chemistry
|March 25, 2010
PubMed

Insights

The embryonic lethal abnormal vision (ELAV)-like RNA-binding protein HuR stabilizes p27(Kip1) mRNA, impacting cell cycle regulation. This study reveals HuR

Area of Science:

  • Molecular Biology
  • Cell Biology
  • RNA Biology

Background:

  • p27(Kip1) is crucial for cell cycle control.
  • Post-transcriptional regulation of p27(Kip1) is complex.
  • The role of HuR in p27(Kip1) translation is debated.

Purpose of the Study:

  • To elucidate the mechanism of HuR in p27(Kip1) regulation.
  • To investigate HuR's role in p27(Kip1) mRNA stability and translation.
  • To identify regulatory elements in p27(Kip1) mRNA.

Main Methods:

  • In vitro and in vivo interaction studies between HuR and p27(Kip1) mRNA.
  • Analysis of U-rich elements in 5' and 3' UTRs of p27(Kip1) mRNA.
  • HuR knockdown and deletion of binding sites experiments.
  • Identification of a CT repeat element in the 5' UTR.

Main Results:

  • HuR binds to U-rich elements in p27(Kip1) mRNA's 5' and 3' UTRs.
  • HuR binding stabilizes p27(Kip1) mRNA, increasing its accumulation.
  • HuR knockdown or deletion of binding sites destabilizes p27(Kip1) mRNA.
  • A CT repeat in the 5' UTR represses p27(Kip1) expression via translation.

Conclusions:

  • HuR primarily regulates p27(Kip1) expression through mRNA stability.
  • HuR-independent mechanisms involving translation also regulate p27(Kip1).
  • This study clarifies the dual role of HuR in p27(Kip1) post-transcriptional regulation.

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