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您的检索式：作者名="Tsan Sam Xiao"
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| 1 | Post-translational regulation of inflammasomes显示文摘在对微生物引起的感染的有免疫力的保护的 Inflammasomes 戏必需品角色。然而,过多的发炎在各种各样的人的疾病被含有,包括 autoinflammatory 症候群,糖尿病,多重硬化,心血管的混乱和 neurodegenerative 疾病。因此,当限制并行的织物损坏时, inflammasome 活动的精确规定为足够的有免疫力的保护是批评的。在这评论,我们集中于调整 NLRP3, NLRP1, NLRC4, AIM2 和 IFI16 inflammasomes 的激活的 translational 以后修正(PTM ) 的新兴的角色。我们预计 PTM 的这些类型将在另外的类型和更少的描绘得好的 inflammasomes 被识别。因为这些高度多样、万用的 PTM 响应感染和织物损坏塑造不同煽动性的回答,指向酶在这些包含了 PTM 将无疑在各种各样的 pathophysiological 条件下面为 inflammasome 活动的精确调整提供机会。 | Jie Yang Zhonghua Liu Tsan Sam Xiao | 2017 | Cellular & Molecular Immunology2017，14，1： | 15 |
| 2 | Innate immunity and inflammation显示文摘 | Tsan Sam Xiao | 2017 | Cellular & Molecular Immunology2017，14，1： | 1 |
| 3 | PD-L1 expression is regulated by ATP-binding of the ERBB3 pseudokinase domain显示文摘How PD-L1 expression is regulated in cancer is poorly understood.Here,we report that the ATP-binding activity of ERBB3 pseudokinase regulates PD-L1 gene expression in colorectal cancers(CRCs).ERBB3 is one of the four members of the EGF receptor family,all with protein tyrosine kinase domains.ERBB3 is a pseudokinase with a high binding affin-ity to ATP.We showed that ERBB3 ATP-binding inactivation mutant reduces tumorigenicity in genetically engineered mouse models and impairs xenograft tumor growth of CRC cell lines.The ERBB3 ATP-binding mutant cells dramatically reduce IFN-g-induced PD-L1 expres-sion.Mechanistically,ERBB3 regulates IFN-g-induced PD-L1 expression through the IRS1-PI3K-PDK1-RSK-CREB signaling axis.CREB is the transcription factor that regulates PD-L1 gene expression in CRC cells.Knockin of a tumor-derived ERBB3 mutation located in the ki-nase domain sensitizes mouse colon cancers to anti-PD1 antibody therapy,suggesting that ERBB3 mutations could be predictive biomarkers for tumors amenable to immune check-point therapy. | Yamu Li Zhonghua Liu Yiqing Zhao Jie Yang Tsan Sam Xiao Ronald A.Conlon Zhenghe Wang | 2023 | Genes & Diseases2023，10，4： | 0 |
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