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by fed-batch systems, but the acute effect may rather be intrinsically triggered and require pharmacological target- ing, in this case NF-κB pathway inhibition, to be reduced. Our finding that targeting NF-κB signaling further enhances HSPC expansion driven by other compounds suggests that this should be further exploited in strategies aimed at HSC expansion for clinical benefit.
Acknowledgments
The authors are thankful to the technical staff and manage-
ment at the Division of Molecular Medicine and Gene Therapy, The Lund Stem Cell Center FACS and Vector cores, as well as the Animal facility at the Biomedical Center. This work was funded by grants from the Swedish Research Council, the Swedish Cancer Foundation, the Swedish Pediatric Cancer Foundation and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation pro- gram (grant agreement n. 648894) to JL. The work was further supported by the HematoLinné and StemTherapy programs at Lund University.
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