Cellular and Molecular Life Sciences CMLS

, Volume 58, Issue 2, pp 266-277

First online:

HuR and mRNA stability

  • C. M. BrennanAffiliated withDepartment of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven (Connecticut 06536, USA), Fax +1 203 624 8213, e-mail: joan.steitz@yale.edu
  • , J. A. Steitz*Affiliated withDepartment of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, 295 Congress Avenue, New Haven (Connecticut 06536, USA), Fax +1 203 624 8213, e-mail: joan.steitz@yale.edu

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Abstract.

An important mechanism of posttranscriptional gene regulation in mammalian cells is the rapid degradation of messenger RNAs (mRNAs) signaled by AU-rich elements (AREs) in their 3′ untranslated regions. HuR, a ubiquitously expressed member of the Hu family of RNA-binding proteins related to Drosophila ELAV, selectively binds AREs and stabilizes ARE-containing mRNAs when overexpressed in cultured cells. This review discusses mRNA decay as a general form of gene regulation, decay signaled by AREs, and the role of HuR and its Hu-family relatives in antagonizing this mRNA degradation pathway. The influence of newly identified protein ligands to HuR on HuR function in both normal and stressed cells may explain how ARE-mediated mRNA decay is regulated in response to environmental change.

Key words. AU-rich element; ELAV; Hu proteins; stress; nuclear export; mRNA stability.