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G-CSF regulates hematopoietic stem cell activity, in part, through activation of toll-like receptor signaling

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1c,d) and was previously suggested as a candidate for a potential activator site, first, because its positive charge might stabilize or bind GSH as GS , and, second, because of its evolutionary conserved position that is equivalent to the GSH-interacting catalytic residue of glutathione transferases 3