ERK5 regulation in naïve T-cell activation and survival

Olga Ananieva, Andrew Macdonald, Xin Wang, Claire E. McCoy, Joanne McIlrath, Cathy Tournier, J. Simon C Arthur

    Research output: Contribution to journalArticlepeer-review


    ERKS has been implicated in regulating the MEF2-dependent genes Klf2 and nur77 downstream of the TCR and the maintenance of expression of CD62L on peripheral T cells. Based on this data, knockout of ERK5 would be predicted to compromise T-cell development and the maintenance of T cells in the periphery. Using an ERK5 conditional knockout, driven by CD4-CRE or Vav-CRE transgenes resulting in the loss of ERK5 in T cells, we have found that ERK5 is not required for T-cell development. In addition, normal numbers of T cells were found in the spleens and lymph nodes of these mice. We also find that TCR stimulation is not a strong signal for ERK5 activation in primary murine T cells. ERK5 was found to contribute to the induction of Klf2 but not nur77 mRNA following TCR activation. Despite the reduction in klf2 mRNA, no effect was seen in ERK5 knockouts on either the mRNA levels for the Klf2 target genes CD62L, CCR7 and S1P, or the cell surface expression of CD62L. These results suggest that while ERK5 does contribute to Klf2 regulation in T cells, it is not essential for the expression of CD62L or T-cell survival. © 2008 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
    Original languageEnglish
    Pages (from-to)2534-2547
    Number of pages13
    JournalEuropean journal of immunology
    Issue number9
    Publication statusPublished - Sept 2008


    • Kinases
    • Klf2
    • MAPK
    • Signal transduction
    • T cells


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