Proteasome-independent degradation of canonical NFkappaB complex components by the NleC protein of pathogenic Escherichia coli.
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Subverting Toll-Like Receptor Signaling by Bacterial PathogensA Family of Salmonella Type III Secretion Effector Proteins Selectively Targets the NF-κB Signaling Pathway to Preserve Host HomeostasisThe Structure and Specificity of the Type III Secretion System Effector NleC Suggest a DNA Mimicry Mechanism of Substrate RecognitionStructure and mechanism of a type III secretion protease, NleCModulation of the Inflammasome Signaling Pathway by Enteropathogenic and Enterohemorrhagic Escherichia coliModulation of the host innate immune and inflammatory response by translocated bacterial proteinsThe enteropathogenic E. coli (EPEC) Tir effector inhibits NF-κB activity by targeting TNFα receptor-associated factorsEscherichia coli and the mucosal immune system.Bortezomib treatment produces nocifensive behavior and changes in the expression of TRPV1, CGRP, and substance P in the rat DRG, spinal cord, and sciatic nerve.Enteropathogenic and enterohaemorrhagic Escherichia coli: even more subversive elements.Functional differences and interactions between the Escherichia coli type III secretion system effectors NleH1 and NleH2.Lysogeny with Shiga toxin 2-encoding bacteriophages represses type III secretion in enterohemorrhagic Escherichia coli.The apoptogenic toxin AIP56 is a metalloprotease A-B toxin that cleaves NF-κb P65Microbial strategies for antagonizing Toll-like-receptor signal transduction.Metalloprotease NleC suppresses host NF-κB/inflammatory responses by cleaving p65 and interfering with the p65/RPS3 interactionAttaching and effacing bacterial effector NleC suppresses epithelial inflammatory responses by inhibiting NF-κB and p38 mitogen-activated protein kinase activation.A type III effector protease NleC from enteropathogenic Escherichia coli targets NF-κB for degradationInhibition of Nuclear Transport of NF-ĸB p65 by the Salmonella Type III Secretion System Effector SpvD.The Type III Effector NleD from Enteropathogenic Escherichia coli Differentiates between Host Substrates p38 and JNK.Identification of an N-terminal truncation of the NF-κB p65 subunit that specifically modulates ribosomal protein S3-dependent NF-κB gene expression.Interference with nuclear factor kappaB signaling pathway by pathogen-encoded proteases: global and selective inhibition.Escherichia coli virulence protein NleH1 interaction with the v-Crk sarcoma virus CT10 oncogene-like protein (CRKL) governs NleH1 inhibition of the ribosomal protein S3 (RPS3)/nuclear factor κB (NF-κB) pathway.Always one step ahead: How pathogenic bacteria use the type III secretion system to manipulate the intestinal mucosal immune system.Ribosomal protein s3: a multifunctional target of attaching/effacing bacterial pathogens.Subversion of innate immune responses by bacterial hindrance of NF-κB pathway.The impact of Toll-like receptors on bacterial virulence strategies.Bacterial interference with canonical NFκB signalling.The cell death response to enteropathogenic Escherichia coli infection.Hijacking of death receptor signaling by bacterial pathogen effectors.Bringing down the host: enteropathogenic and enterohaemorrhagic Escherichia coli effector-mediated subversion of host innate immune pathways.Role of virulence factors on host inflammatory response induced by diarrheagenic Escherichia coli pathotypes.T3SS-Independent Uptake of the Short-Trip Toxin-Related Recombinant NleC Effector of Enteropathogenic Escherichia coli Leads to NF-κB p65 Cleavage.Epithelial cells detect functional type III secretion system of enteropathogenic Escherichia coli through a novel NF-κB signaling pathway.Distinct Roles of the Antiapoptotic Effectors NleB and NleF from Enteropathogenic Escherichia coliModulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins.The pathogenic Escherichia coli type III secreted protease NleC degrades the host acetyltransferase p300.Down the rabbit hole: Is necroptosis truly an innate response to infection?Identification of a Distinct Substrate-binding Domain in the Bacterial Cysteine Methyltransferase Effectors NleE and OspZ.Substrate recognition by the zinc metalloprotease effector NleC from enteropathogenic Escherichia coli.A distinct regulatory sequence is essential for the expression of a subset of nle genes in attaching and effacing Escherichia coli.
P2860
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P2860
Proteasome-independent degradation of canonical NFkappaB complex components by the NleC protein of pathogenic Escherichia coli.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
@zh
2010年论文
@zh-cn
name
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@en
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@nl
type
label
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@en
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@nl
prefLabel
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@en
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@nl
P2093
P2860
P356
P1476
Proteasome-independent degrada ...... f pathogenic Escherichia coli.
@en
P2093
Brendan Kenny
Marie-Hélène Ruchaud-Sparagano
Sabrina Mühlen
P2860
P304
P356
10.1074/JBC.M110.172254
P407
P577
2010-12-09T00:00:00Z