NDLI: Cutting Edge : TNF-- Converting Enzyme ( TACE / ADAM 17 ) Inactivation in Mouse Myeloid Cells Prevents Lethality from Endotoxin Shock 1

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Cutting Edge : TNF-- Converting Enzyme ( TACE / ADAM 17 ) Inactivation in Mouse Myeloid Cells Prevents Lethality from Endotoxin Shock 1

Content Provider	Semantic Scholar
Author	Horiuchi, Keisuke Kimura, Tokuhiro Miyamoto, Takeshi Takaishi, Hironari Okada, Yasunori Toyama, Yoshiaki Blobel, Carl P.
Copyright Year	2007
Abstract	TNF, a potent proinflammatory cytokine, is synthesized as a membrane-anchored precursor and proteolytically released from cells. Soluble TNF is the primary mediator of pathologies such as rheumatoid arthritis, Crohn’s disease, and endotoxin shock. The TNFconverting enzyme (TACE), a disintegrin and metalloprotease 17 (ADAM17), has emerged as the best candidate TNF sheddase, but other proteinases can also release TNF. Because TACE-deficient mice die shortly after birth, we generated conditional TACE-deficient mice to address whether TACE is the relevant sheddase for TNF in adult mice. In this study, we report that TACE inactivation in myeloid cells or temporal inactivation at 6 wk offers strong protection from endotoxin shock lethality in mice by preventing increased TNF serum levels. These findings corroborate that TACE is the major endotoxin-stimulated TNF sheddase in mouse myeloid cells in vivo, thereby further validating TACE as a principal target for the treatment of TNF-dependent pathologies. The Journal of Immunology, 2007, 179: 2686–2689.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://pbsb.med.cornell.edu/pdfs/Horiuchi_JI.pdf
Alternate Webpage(s)	http://pbsb.med.cornell.edu/pdfs/HoriuchiJI.pdf
Language	English
Access Restriction	Open
Subject Keyword	ADAM17 gene ADAM17 protein, human Crohn Disease Electroconvulsive Therapy Endopeptidases Heat-Shock Proteins 70 Mediator brand of benfluorex hydrochloride Metalloproteases Rheumatoid Arthritis Shock Tissue membrane Transarterial Chemoembolization Video-in video-out cytokine
Content Type	Text
Resource Type	Article

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