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This is because mice lacking NOX2 exhibit lower levels of oxidative burst and are less vulnerable to experimentally induced UC (133)

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doi: 10.1126/science.aav9776 218 Maor-NofM.ShiponyZ.Lopez-GonzalezR.NakayamaL.ZhangY

Conclusion The modified nano-product (TLR2 pep-orid-liposome) with structural encapsulation, efficiency enhancement and specific targeting of oridonin demonstrate the potential to a candidate for AML therapeutics