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Rapidly altering 3-O-sulfation provides a cellular mechanism to modulate the response to FGFR2b signaling and control progenitor expansion. Model showing that 3-O-HS rapidly increases 3-O-sulfotranseferase expression, 3-O-sulfated HS on the epithelium and FGF10/FGFR2b complex formation, MAPK signaling, gene expression of FGFR2b signaling targets, proliferation genes, and Kit and its ligand, which expands the KIT+FGFR2b+ progenitors.
