Adam17-dependent shedding limits early neutrophil influx but does not alter early monocyte recruitment to inflammatory sites.
about
A Disintegrin and Metalloprotease 17 in the Cardiovascular and Central Nervous SystemsEGF receptor is required for KRAS-induced pancreatic tumorigenesisL-selectin shedding is activated specifically within transmigrating pseudopods of monocytes to regulate cell polarity in vitro.Ectodomain Shedding by ADAM17: Its Role in Neutrophil Recruitment and the Impairment of This Process during SepsisADAM9 is a novel product of polymorphonuclear neutrophils: regulation of expression and contributions to extracellular matrix protein degradation during acute lung injury.Francisella tularensis subsp. tularensis induces a unique pulmonary inflammatory response: role of bacterial gene expression in temporal regulation of host defense responsesRegulation of CXCR2 expression and function by a disintegrin and metalloprotease-17 (ADAM17).Metalloproteinase-mediated Shedding of Integrin β2 promotes macrophage efflux from inflammatory sites.Mast cell-mediated inhibition of abdominal neutrophil inflammation by a PEGylated TLR7 ligand.Loss of ADAM17-Mediated Tumor Necrosis Factor Alpha Signaling in Intestinal Cells Attenuates Mucosal Atrophy in a Mouse Model of Parenteral NutritionADAM17 activation in circulating neutrophils following bacterial challenge impairs their recruitment.Monocyte ADAM17 promotes diapedesis during transendothelial migration: identification of steps and substrates targeted by metalloproteinasesEndothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults.Ectoenzymes controlling leukocyte traffic.ADAM-family metalloproteinases in lung inflammation: potential therapeutic targets.Fine Tuning Cell Migration by a Disintegrin and Metalloproteinases.Resolution of inflammation pathways in preeclampsia-a narrative review.The role of ADAM17 in the T-cell response against bacterial pathogens.Targeting ADAM17 in leukocytes increases neutrophil recruitment and reduces bacterial spread during polymicrobial sepsis.Macrophage ADAM17 deficiency augments CD36-dependent apoptotic cell uptake and the linked anti-inflammatory phenotype.Hypercapnia attenuates ventilator-induced lung injury via a disintegrin and metalloprotease-17.A head-to-tail view of L-selectin and its impact on neutrophil behaviour.
P2860
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P2860
Adam17-dependent shedding limits early neutrophil influx but does not alter early monocyte recruitment to inflammatory sites.
description
2011 nî lūn-bûn
@nan
2011 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2011年の論文
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年学术文章
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2011年學術文章
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name
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@ast
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@en
type
label
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@ast
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@en
prefLabel
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@ast
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@en
P2093
P2860
P1433
P1476
Adam17-dependent shedding limi ...... uitment to inflammatory sites.
@en
P2093
Bridgit Bell
Carole L Wilson
Craig T Lefort
Elaine W Raines
Ivan Gomez
Jingjing Tang
Li-Chuan Huang
P2860
P304
P356
10.1182/BLOOD-2010-11-321406
P407
P577
2011-05-31T00:00:00Z