Inhibition of MAPK and NF-kappa B pathways is necessary for rapid apoptosis in macrophages infected with Yersinia.
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Cell death programs in Yersinia immunity and pathogenesisThe human-bacterial pathogen protein interaction networks of Bacillus anthracis, Francisella tularensis, and Yersinia pestisAlveolar macrophage innate response to Mycobacterium immunogenum, the etiological agent of hypersensitivity pneumonitis: role of JNK and p38 MAPK pathwaysYersinia type III effectors perturb host innate immune responsesESX-1-induced apoptosis during mycobacterial infection: to be or not to be, that is the questionTemporal Progression of Pneumonic Plague in Blood of Nonhuman Primate: A Transcriptomic AnalysisIntegrating high-content imaging and chemical genetics to probe host cellular pathways critical for Yersinia pestis infectionStructural mechanism of ubiquitin and NEDD8 deamidation catalyzed by bacterial effectors that induce macrophage-specific apoptosis.Macrophage activation redirects yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis.Reduced secretion of YopJ by Yersinia limits in vivo cell death but enhances bacterial virulence.Yersinia outer protein YopE affects the actin cytoskeleton in Dictyostelium discoideum through targeting of multiple Rho family GTPasesNeutrophils are resistant to Yersinia YopJ/P-induced apoptosis and are protected from ROS-mediated cell death by the type III secretion systemCaspase-8 mediates caspase-1 processing and innate immune defense in response to bacterial blockade of NF-κB and MAPK signalingYopJ-promoted cytotoxicity and systemic colonization are associated with high levels of murine interleukin-18, gamma interferon, and neutrophils in a live vaccine model of Yersinia pseudotuberculosis infectionA Yersinia effector with enhanced inhibitory activity on the NF-κB pathway activates the NLRP3/ASC/caspase-1 inflammasome in macrophagesA Yersinia effector protein promotes virulence by preventing inflammasome recognition of the type III secretion system.Delineation of regions of the Yersinia YopM protein required for interaction with the RSK1 and PRK2 host kinases and their requirement for interleukin-10 production and virulenceTNFalpha up-regulates SLUG via the NF-kappaB/HIF1alpha axis, which imparts breast cancer cells with a stem cell-like phenotype.YopJ-induced caspase-1 activation in Yersinia-infected macrophages: independent of apoptosis, linked to necrosis, dispensable for innate host defense.Acetylation of MEK2 and I kappa B kinase (IKK) activation loop residues by YopJ inhibits signaling.The apoptogenic toxin AIP56 is a metalloprotease A-B toxin that cleaves NF-κb P65How the structural gene products of Yersinia pestis relate to virulence.Interaction of Yersinia pestis with macrophages: limitations in YopJ-dependent apoptosis.Early apoptosis of macrophages modulated by injection of Yersinia pestis YopK promotes progression of primary pneumonic plagueYopP-expressing variant of Y. pestis activates a potent innate immune response affording cross-protection against yersiniosis and tularemia [corrected].Yersinia pestis YopJ suppresses tumor necrosis factor alpha induction and contributes to apoptosis of immune cells in the lymph node but is not required for virulence in a rat model of bubonic plagueFlagellin suppresses epithelial apoptosis and limits disease during enteric infectionInduction of cancer cell death by isoflavone: the role of multiple signaling pathways.SseL, a Salmonella deubiquitinase required for macrophage killing and virulence.Type III secretion system-dependent translocation of ectopically expressed Yop effectors into macrophages by intracellular Yersinia pseudotuberculosis.Pathogenesis of Y. enterocolitica and Y. pseudotuberculosis in Human Yersiniosis.Growth of Yersinia pseudotuberculosis in mice occurs independently of Toll-like receptor 2 expression and induction of interleukin-10.NF-kappaB translocation prevents host cell death after low-dose challenge by Legionella pneumophila.Macrophage cell death upon intracellular bacterial infection.Proteomic profiling of lipopolysaccharide-activated macrophages by isotope coded affinity taggingCaspase-1 activation in macrophages infected with Yersinia pestis KIM requires the type III secretion system effector YopJ.Type III secretion decreases bacterial and host survival following phagocytosis of Yersinia pseudotuberculosis by macrophages.Vibrio parahaemolyticus orchestrates a multifaceted host cell infection by induction of autophagy, cell rounding, and then cell lysis.Staying alive: bacterial inhibition of apoptosis during infection.Innate immune response during Yersinia infection: critical modulation of cell death mechanisms through phagocyte activation.
P2860
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P2860
Inhibition of MAPK and NF-kappa B pathways is necessary for rapid apoptosis in macrophages infected with Yersinia.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
2005年论文
@zh
2005年论文
@zh-cn
name
Inhibition of MAPK and NF-kapp ...... phages infected with Yersinia.
@en
type
label
Inhibition of MAPK and NF-kapp ...... phages infected with Yersinia.
@en
prefLabel
Inhibition of MAPK and NF-kapp ...... phages infected with Yersinia.
@en
P2093
P1476
Inhibition of MAPK and NF-kapp ...... phages infected with Yersinia.
@en
P2093
Adrian T Ting
James B Bliska
Kenneth B Marcu
P304
P356
10.4049/JIMMUNOL.174.12.7939
P407
P577
2005-06-01T00:00:00Z