Figure 6
Scheme of the proposed model. G-CSF administration causes a transient up-regulation of SDF-1,4 (1) which activates CXCR4 signaling (2) crucial for promoting stem cell egress.2,4,20,21 CXCR4/SDF-1 activation leads to an up-regulation of HGF in BM PMN cells. (3) HGF subsequently binds to c-Met and thus promotes its activation. (4) c-Met in turn induces mTOR signaling, (5) which represses FOXO3a. (6) Subsequently, FOXO3a inhibition causes increased ROS production (7); this signaling cascade ultimately promotes hematopoietic stem and progenitor cell egress out of the BM reservoir (8).

Scheme of the proposed model. G-CSF administration causes a transient up-regulation of SDF-1, (1) which activates CXCR4 signaling (2) crucial for promoting stem cell egress.2,4,20,21  CXCR4/SDF-1 activation leads to an up-regulation of HGF in BM PMN cells. (3) HGF subsequently binds to c-Met and thus promotes its activation. (4) c-Met in turn induces mTOR signaling, (5) which represses FOXO3a. (6) Subsequently, FOXO3a inhibition causes increased ROS production (7); this signaling cascade ultimately promotes hematopoietic stem and progenitor cell egress out of the BM reservoir (8).

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