Figure 7
Figure 7. Schematic model of the mechanism of Tak1 protection of HSPC survival. Two distinct populations of HSPCs exist in BM hematopoietic tissue based on their response to TNF-α/Fas-induced death signaling. TNF-α/Fas, acting through RIP-1, stimulates necroptosis in 30% to 40% of HSPCs, whereas (an) unknown factor(s) induce(s) caspase-8–dependent type I or II apoptosis in the remaining HSPCs. Tak1-mediated survival signaling, stimulated by proinflammatory cytokines, prevents both types of cell death.

Schematic model of the mechanism of Tak1 protection of HSPC survival. Two distinct populations of HSPCs exist in BM hematopoietic tissue based on their response to TNF-α/Fas-induced death signaling. TNF-α/Fas, acting through RIP-1, stimulates necroptosis in 30% to 40% of HSPCs, whereas (an) unknown factor(s) induce(s) caspase-8–dependent type I or II apoptosis in the remaining HSPCs. Tak1-mediated survival signaling, stimulated by proinflammatory cytokines, prevents both types of cell death.

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