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.
- Koki Ueda
- Rajni Kumari
- Ulrich Steidl