ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
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Acidic mammalian chitinase is secreted via an ADAM17/epidermal growth factor receptor-dependent pathway and stimulates chemokine production by pulmonary epithelial cellsPhosphatidylserine exposure is required for ADAM17 sheddase functionStructural Insights into Calmodulin-regulated L-selectin Ectodomain SheddingA Disintegrin and Metalloprotease 17 in the Cardiovascular and Central Nervous SystemsGlycosyltransferase-programmed stereosubstitution (GPS) to create HCELL: engineering a roadmap for cell migrationA biosensor for the activity of the "sheddase" TACE (ADAM17) reveals novel and cell type-specific mechanisms of TACE activationMetalloproteolytic receptor shedding…platelets "acting their age".Myeloid-derived suppressor cells down-regulate L-selectin expression on CD4+ and CD8+ T cells.Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the Impairment of This Process during SepsisPhosphatidylinositol-3-OH kinase and nutrient-sensing mTOR pathways control T lymphocyte traffickingADAM17 activity and other mechanisms of soluble L-selectin production during death receptor-induced leukocyte apoptosis.In vivo role of leukocyte ADAM17 in the inflammatory and host responses during E. coli-mediated peritonitisLeukocyte ADAM17 regulates acute pulmonary inflammation.Conditional inactivation of TACE by a Sox9 promoter leads to osteoporosis and increased granulopoiesis via dysregulation of IL-17 and G-CSF.Posttranslational modification of the NH2-terminal region of CXCL5 by proteases or peptidylarginine Deiminases (PAD) differently affects its biological activityInvestigation of the role of TNF-α converting enzyme (TACE) in the inhibition of cell surface and soluble TNF-α production by acute ethanol exposureCD62L (L-selectin) shedding for assessment of perioperative immune sensitivity in patients undergoing cardiac surgery with cardiopulmonary bypass.Cord blood neutrophils display a galectin-3 responsive phenotype accentuated by vaginal delivery.Regulation of CXCR2 expression and function by a disintegrin and metalloprotease-17 (ADAM17).Identification of an ADAM17 cleavage region in human CD16 (FcγRIII) and the engineering of a non-cleavable version of the receptor in NK cells.Different signaling pathways stimulate a disintegrin and metalloprotease-17 (ADAM17) in neutrophils during apoptosis and activation.iRhoms 1 and 2 are essential upstream regulators of ADAM17-dependent EGFR signalingEngineering cellular trafficking via glycosyltransferase-programmed stereosubstitutionADAM17 activation in circulating neutrophils following bacterial challenge impairs their recruitment.ADAM17 cleaves CD16b (FcγRIIIb) in human neutrophilsLeukocyte cell surface proteinases: regulation of expression, functions, and mechanisms of surface localization.NK cell CD16 surface expression and function is regulated by a disintegrin and metalloprotease-17 (ADAM17).Myeloid-derived suppressor cells: more mechanisms for inhibiting antitumor immunity.Regulation of mature ADAM17 by redox agents for L-selectin sheddingADAMs 10 and 17 represent differentially regulated components of a general shedding machinery for membrane proteins such as transforming growth factor alpha, L-selectin, and tumor necrosis factor alpha.ADAM17 in tumor associated leukocytes regulates inflammatory mediators and promotes mammary tumor formation.FERM domain of moesin desorbs the basic-rich cytoplasmic domain of l-selectin from the anionic membrane surface.Cutaneous lymphocyte-associated antigen (CLA) T cells up-regulate P-selectin ligand expression upon their activationTumor-induced MDSC act via remote control to inhibit L-selectin-dependent adaptive immunity in lymph nodes.The immunobiology of myeloid-derived suppressor cells in cancer.Neutrophil-derived JAML inhibits repair of intestinal epithelial injury during acute inflammation.Melittin modulates keratinocyte function through P2 receptor-dependent ADAM activation.Down-Regulation of CD62L Shedding in T Cells by CD39+ Regulatory T Cells Leads to Defective Sensitization in Contact Hypersensitivity Reactions.Targeting ADAM17 in leukocytes increases neutrophil recruitment and reduces bacterial spread during polymicrobial sepsis.ADAM17 controls IL-6 signaling by cleavage of the murine IL-6Rα from the cell surface of leukocytes during inflammatory responses.
P2860
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P2860
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
description
2006 nî lūn-bûn
@nan
2006 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@ast
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@en
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@nl
type
label
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@ast
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@en
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@nl
prefLabel
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@ast
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@en
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@nl
P2093
P2860
P3181
P1433
P1476
ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding
@en
P2093
Amy Herrera
Bruce Walcheck
Jennifer Brazzell
P2860
P304
P3181
P356
10.1182/BLOOD-2006-02-005827
P407
P577
2006-10-01T00:00:00Z