UAP56 is a novel interacting partner of Bcr in regulating vascular smooth muscle cell DNA synthesis

Abha Sahni, Nadan Wang, Jeffrey D. Alexis

Research output: Contribution to journalArticle

2 Scopus citations


Bcr is a serine/threonine kinase that is a critical regulator of vascular smooth muscle cell inflammation and proliferation. We have previously demonstrated that Bcr acts in part via phosphorylation and inhibition of PPARγ. We have identified the RNA helicase UAP56 as another substrate of Bcr. In this report we demonstrate that knockdown of UAP56 blocks Bcr induced DNA synthesis in vascular smooth muscle cells (VSMC). We also found that over expression of Bcr increased the expression of cyclin E and decreased the expression of p27. Knockdown of UAP56 reversed the effect of Bcr on cyclin E and p27 expression. Furthermore, we found that Bcr binds to UAP56 and demonstrate that binding of UAP56 to Bcr is critical for Bcr induced DNA synthesis in VSMC. Our data identify UAP56 as an important binding partner of Bcr and a novel target for inhibiting vascular smooth muscle cell proliferation.

Original languageEnglish (US)
Pages (from-to)511-515
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Apr 13 2012



  • DExD/H box protein
  • DNA synthesis
  • RNA helicase

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology

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