Abstract
By exploiting a congenic pair of induced pluripotent stem cell (iPSC) lines derived from a familial platelet disorder (FPD) patient, 1 harboring a monoallelic mutation in RUNX1 and the other a corrected allele, in this issue of Blood, Li et al have discovered that negative regulation of NOTCH4 by RUNX1 is required for normal human megakaryocyte (MK) development. Furthermore, the authors demonstrate that suppressing NOTCH signaling, by either genetic or chemical perturbation, significantly enhances MK yield.
MeSH terms
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Core Binding Factor Alpha 2 Subunit*
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Hematopoiesis
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Humans
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Megakaryocytes*
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Receptor, Notch4
Substances
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Core Binding Factor Alpha 2 Subunit
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NOTCH4 protein, human
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Receptor, Notch4