AU-rich elements and associated factors: are there unifying principles?

AU-rich elements and associated factors: are there unifying principles?

Received September 17, 2005; Revised November 5, 2005; Accepted November 25, 2005 | Carine Barreau, Luc Paillard and H. Beverley Osborne*
The article reviews the control of mRNA stability through AU-rich elements (AREs) and the associated binding proteins (ARE-BPs). AREs, rich in adenosine and uridine nucleotides, target mRNAs for rapid degradation, often in response to stress or inflammatory stimuli. The review highlights the sequence characteristics of AREs and the known ARE-BPs, including their effects on mRNA stability and translation. It discusses the multiplicity of ARE-BP-mRNA associations, suggesting functional redundancies or antagonisms. The role of ARE-BPs in mRNA degradation is explored, with a focus on AUFI, the Hu family (HuR, Hel-N1, HuC, HuD), and TTP. The mechanisms of ARE-dependent degradation, including rapid deadenylation and the involvement of the exosome and P-bodies, are discussed. The coupling of ARE-dependent degradation and translation is also examined, with evidence for both positive and negative regulatory roles. The article concludes by proposing unifying principles that could integrate the diverse data on AREs and ARE-BPs, emphasizing the need for further research to understand the complex regulatory pathways involved.The article reviews the control of mRNA stability through AU-rich elements (AREs) and the associated binding proteins (ARE-BPs). AREs, rich in adenosine and uridine nucleotides, target mRNAs for rapid degradation, often in response to stress or inflammatory stimuli. The review highlights the sequence characteristics of AREs and the known ARE-BPs, including their effects on mRNA stability and translation. It discusses the multiplicity of ARE-BP-mRNA associations, suggesting functional redundancies or antagonisms. The role of ARE-BPs in mRNA degradation is explored, with a focus on AUFI, the Hu family (HuR, Hel-N1, HuC, HuD), and TTP. The mechanisms of ARE-dependent degradation, including rapid deadenylation and the involvement of the exosome and P-bodies, are discussed. The coupling of ARE-dependent degradation and translation is also examined, with evidence for both positive and negative regulatory roles. The article concludes by proposing unifying principles that could integrate the diverse data on AREs and ARE-BPs, emphasizing the need for further research to understand the complex regulatory pathways involved.
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