FasL expression in activated T lymphocytes involves HuR-mediated stabilization

Gillian L. Drury, Sergio Di Marco, Virginie Dormoy-Raclet, Julie Desbarats, Imed Eddine Gallouzi

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


A prolonged activation of the immune system is one of the main causes of hyperproliferation of lymphocytes leading to defects in immune tolerance and autoimmune diseases. Fas ligand (FasL), a member of the TNF superfamily, plays a crucial role in controlling this excessive lymphoproliferation by inducing apoptosis in T cells leading to their rapid elimination. Here, we establish that posttranscriptional regulation is part of the molecular mechanisms that modulate FasL expression, and we show that in activated T cells FasL mRNA is stable. Our sequence analysis indicates that the FasL 3′-untranslated region (UTR) contains two AU-rich elements (AREs) that are similar in sequence and structure to those present in the 3′-UTR of TNFα mRNA. Through these AREs, the FasL mRNA forms a complex with the RNA-binding protein HuR both in vitro and ex vivo. Knocking down HuR in HEK 293 cells prevented the phorbol 12-myristate 13-acetate-induced expression of a GFP reporter construct fused to the FasL 3′-UTR. Collectively, our data demonstrate that the posttranscriptional regulation of FasL mRNA by HuR represents a novel mechanism that could play a key role in the maintenance and proper functioning of the immune system. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
Original languageEnglish (US)
Pages (from-to)31130-31138
Number of pages9
JournalJournal of Biological Chemistry
Issue number41
StatePublished - Oct 8 2010
Externally publishedYes

Bibliographical note

Generated from Scopus record by KAUST IRTS on 2022-09-13

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology


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