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Fueling clonal dominance through TRAFficking of NF-κB signaling

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Activation of TLR–TRAF6 signaling by chronic inflammation in myelodysplastic syndromes increases the competitive advantage of HSPCs harboring MDS mutations through the upregulation of the ubiquitin-modifying enzyme A20 and a switch from canonical to non-canonical NF-κB signaling.

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Fig. 1: Overexpression of TRAF6 and systemic inflammation support clonal dominance in MDS.

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Author notes

  1. These authors contributed equally: Koki Ueda, Rajni Kumari.

Authors and Affiliations

  1. Department of Cell Biology, Albert Einstein College of Medicine, New York, NY, USA

    Koki Ueda, Rajni Kumari & Ulrich Steidl

  2. Ruth L. and David S. Gottesman Institute for Stem Cell Research and Regenerative Medicine, Albert Einstein College of Medicine, New York, NY, USA

    Koki Ueda, Rajni Kumari & Ulrich Steidl

  3. Department of Medicine (Oncology), Albert Einstein College of Medicine — Montefiore Medical Center, New York, NY, USA

    Ulrich Steidl

  4. Albert Einstein Cancer Center, Albert Einstein College of Medicine, New York, NY, USA

    Ulrich Steidl

Authors
  1. Koki Ueda
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  2. Rajni Kumari
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  3. Ulrich Steidl
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Corresponding author

Correspondence to Ulrich Steidl.

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The authors declare no competing interests.

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Ueda, K., Kumari, R. & Steidl, U. Fueling clonal dominance through TRAFficking of NF-κB signaling. Nat Immunol 21, 489–490 (2020). https://doi.org/10.1038/s41590-020-0662-0

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