IndraLab

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USP6 activates CXCL10. 5 / 5
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"To further test this feedforward model, we sought to confirm whether CXCL9/CXCL10 were produced by the USP6/RD-ES cells, because NK cells are also capable of producing these chemokines (29, 34–36)."
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eidos
"As shown in Figure 2C , the first STAT1 site , both NF-kappaB sites , and the ISRE all contributed to activation of the CXCL10 promoter by USP6 + IFNgamma , whereas the AP-1 site was largely dispensable ."
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eidos
"This study demonstrates that high USP6 expression is associated with all of these hot TME hallmarks in ES patients , and that USP6 is sufficient to drive an IFN response signature and CXCL10 expression in vitro , as well as intra-tumoral immune cell recruitment and activation in vivo ."
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"USP6 also triggered surface stabilization of the type I and type II IFN receptors, IFNAR1 and IFNGR1, rendering Ewing sarcoma cells hyperresponsive to ectopic IFNs with resultant synergistic induction of IFN response genes, including CXCL10 (20)."
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"Upon activation, NK cells secrete IFNγ, which feeds back on USP6-expressing Ewing sarcoma cells to synergistically induce CXCL9/CXCL10."
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