CELFish ways to modulate mRNA decay

Irina Vlasova-St. Louis, Alexa M. Dickson, Paul R. Bohjanen, Carol J. Wilusz

Research output: Contribution to journalReview articlepeer-review

37 Scopus citations


The CELF family of RNA-binding proteins regulates many steps of mRNA metabolism. Although their best characterized function is in pre-mRNA splice site choice, CELF family members are also powerful modulators of mRNA decay. In this review we focus on the different modes of regulation that CELF proteins employ to mediate mRNA decay by binding to GU-rich elements. After starting with an overview of the importance of CELF proteins during development and disease pathogenesis, we then review the mRNA networks and cellular pathways these proteins regulate and the mechanisms by which they influence mRNA decay. Finally, we discuss how CELF protein activity is modulated during development and in response to cellular signals. We conclude by highlighting the priorities for new experiments in this field. This article is part of a Special Issue entitled: RNA Decay mechanisms.

Original languageEnglish (US)
Pages (from-to)695-707
Number of pages13
JournalBiochimica et Biophysica Acta - Gene Regulatory Mechanisms
Issue number6-7
StatePublished - Jun 2013

Bibliographical note

Funding Information:
C.J.W. is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number AR059247 . P.R.B. and I.A.V-S. are supported by NIH grant AI072068 . A.M.D. is supported by a post-doctoral fellowship from the Myotonic Dystrophy Foundation . The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or the Myotonic Dystrophy Foundation. We thank Dr. Ying Zhang (University of Minnesota Supercomputing Institute) and Dr. Eric Ross (Colorado State University) for helpful discussions regarding protein structures and prion domains.


  • CELF (CUGBP ELAV-Like Family) protein
  • Deadenylation
  • ELAV
  • GU-rich element
  • MRNA decay
  • Myotonic dystrophy


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