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Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells

Author

Listed:
  • Kai Fu

    (Bloomberg School of Public Health, Johns Hopkins University)

  • Xin Sun

    (Bloomberg School of Public Health, Johns Hopkins University)

  • Wenxin Zheng

    (Bloomberg School of Public Health, Johns Hopkins University)

  • Eric M. Wier

    (Bloomberg School of Public Health, Johns Hopkins University)

  • Andrea Hodgson

    (Bloomberg School of Public Health, Johns Hopkins University)

  • Dat Q. Tran

    (University of Texas-Houston Medical School)

  • Stéphane Richard

    (Terry Fox Molecular Oncology Group and the Bloomfield Center for Research on Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital
    McGill University
    McGill University)

  • Fengyi Wan

    (Bloomberg School of Public Health, Johns Hopkins University)

Abstract

CD25, the alpha chain of the interleukin-2 receptor, is expressed in activated T cells and has a significant role in autoimmune disease and tumorigenesis; however, the mechanisms regulating transcription of CD25 remain elusive. Here we identify the Src-associated substrate during mitosis of 68 kDa (Sam68) as a novel non-Rel component in the nuclear factor-kappaB (NF-κB) complex that confers CD25 transcription. Our results demonstrate that Sam68 has an essential role in the induction and maintenance of CD25 in T cells. T-cell receptor engagement triggers translocation of the inhibitor of NF-κB kinase alpha (IKKα) from the cytoplasm to the nucleus, where it phosphorylates Sam68, causing complex formation with NF-κB in the nucleus. These findings reveal the important roles of KH domain-containing components and their spatial interactions with IKKs in determining the binding targets of NF-κB complexes, thus shedding novel insights into the regulatory specificity of NF-κB.

Suggested Citation

  • Kai Fu & Xin Sun & Wenxin Zheng & Eric M. Wier & Andrea Hodgson & Dat Q. Tran & Stéphane Richard & Fengyi Wan, 2013. "Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells," Nature Communications, Nature, vol. 4(1), pages 1-11, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2916
    DOI: 10.1038/ncomms2916
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