Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death

doi:10.1126/science.aau2818

GSTDTAP > 地球科学

DOI	10.1126/science.aau2818
	Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death
	Orning, Pontus 1,2; Weng, Dan 1,3; Starheim, Kristian 1,2; Ratner, Dmitry 1; Best, Zachary 1; Lee, Bettina 4; Brooks, Alexandria 1; Xia, Shiyu 5,6; Wu, Hao 5,6; Kelliher, Michelle A.7; Berger, Scott B.8; Gough, Peter J.8; Bertin, John 8; Proulx, Megan M.9; Goguen, Jon D.9; Kayagaki, Nobuhiko 4; Fitzgerald, Katherine A.2; Lien, Egil 1,2
	2018-11-30
发表期刊	SCIENCE
ISSN	0036-8075
EISSN	1095-9203
出版年	2018
卷号	362 期号:6418 页码:1064-+
文章类型	Article
语种	英语
国家	USA; Norway; Peoples R China
英文摘要	Limited proteolysis of gasdermin D (GSDMD) generates an N-terminal pore-forming fragment that controls pyroptosis in macrophages. GSDMD is processed via inflammasome-activated caspase-1 or -11. It is currently unknown whether macrophage GSDMD can be processed by other mechanisms. Here, we describe an additional pathway controlling GSDMD processing. The inhibition of TAK1 or I kappa B kinase (IKK) by the Yersinia effector protein YopJ elicits RIPK1- and caspase-8-dependent cleavage of GSDMD, which subsequently results in cell death. GSDMD processing also contributes to the NLRP3 inflammasome-dependent release of interleukin-1 beta (IL-1 beta). Thus, caspase-8 acts as a regulator of GSDMD-driven cell death. Furthermore, this study establishes the importance of TAK1 and IKK activity in the control of GSDMD cleavage and cytotoxicity.
领域	地球科学 ; 气候变化 ; 资源环境
收录类别	SCI-E
WOS记录号	WOS:000451609000048
WOS关键词	NF-KAPPA-B ; YERSINIA-PESTIS ; ACTIVATION ; CASPASE-1 ; PYROPTOSIS ; NECROSIS ; GSDMD ; TRIF ; PHOSPHORYLATION ; COLONIZATION
WOS类目	Multidisciplinary Sciences
WOS研究方向	Science & Technology - Other Topics
引用统计
文献类型	期刊论文
条目标识符	http://119.78.100.173/C666/handle/2XK7JSWQ/200194
专题	地球科学资源环境科学气候变化
作者单位	1.Univ Massachusetts, Div Infect Dis & Immunol, Dept Med, Program Innate Immun,Med Sch, Worcester, MA 01605 USA; 2.Norwegian Univ Sci & Technol, Dept Clin & Mol Med, Ctr Mol Inflammat Res, N-7491 Trondheim, Norway; 3.Nanjing Univ Sci & Technol, Ctr Mol Metab, Nanjing 210094, Jiangsu, Peoples R China; 4.Genentech Inc, Dept Physiol Chem, San Francisco, CA 94080 USA; 5.Harvard Med Sch, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA; 6.Boston Childrens Hosp, Program Cellular & Mol Med, Boston, MA 02115 USA; 7.Univ Massachusetts, Dept Canc Biol, Med Sch, Worcester, MA 01605 USA; 8.GlaxoSmithKline, Pattern Recognit Receptor Discovery Performance U, Immunoinflammat Therapeut Area, Collegeville, PA 19426 USA; 9.Univ Massachusetts, Dept Microbiol & Physiol, Med Sch, Worcester, MA 01655 USA
推荐引用方式 GB/T 7714	Orning, Pontus,Weng, Dan,Starheim, Kristian,et al. Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death[J]. SCIENCE,2018,362(6418):1064-+.
APA	Orning, Pontus.,Weng, Dan.,Starheim, Kristian.,Ratner, Dmitry.,Best, Zachary.,...&Lien, Egil.(2018).Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death.SCIENCE,362(6418),1064-+.
MLA	Orning, Pontus,et al."Pathogen blockade of TAK1 triggers caspase-8-dependent cleavage of gasdermin D and cell death".SCIENCE 362.6418(2018):1064-+.