Clostridium difficile Toxin B causes epithelial cell necrosis through an autoprocessing-independent mechanism
about
Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal EffectsReactive Oxygen Species as Additional Determinants for Cytotoxicity of Clostridium difficile Toxins A and BThe Role of Rho GTPases in Toxicity of Clostridium difficile ToxinsHost recognition of Clostridium difficile and the innate immune response.Glucosylation Drives the Innate Inflammatory Response to Clostridium difficile Toxin AHigh temporal resolution of glucosyltransferase dependent and independent effects of Clostridium difficile toxins across multiple cell types.Inflammasome activation contributes to interleukin-23 production in response to Clostridium difficile.Coronaviruses induce entry-independent, continuous macropinocytosisUtility of Clostridium difficile toxin B for inducing anti-tumor immunity.Translocation domain mutations affecting cellular toxicity identify the Clostridium difficile toxin B pore.Human defensins facilitate local unfolding of thermodynamically unstable regions of bacterial protein toxins.Critical roles of Clostridium difficile toxin B enzymatic activities in pathogenesis.Exposure of neutralizing epitopes in the carboxyl-terminal domain of TcdB is altered by a proximal hypervariable region.Chondroitin sulfate proteoglycan 4 functions as the cellular receptor for Clostridium difficile toxin B.Clostridium difficile toxin B intoxicated mouse colonic epithelial CT26 cells stimulate the activation of dendritic cells.Distinct roles of the repeat-containing regions and effector domains of the Vibrio vulnificus multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin.Identification of an epithelial cell receptor responsible for Clostridium difficile TcdB-induced cytotoxicity.Precision medicine in alcoholic and nonalcoholic fatty liver disease via modulating the gut microbiota.Glucosyltransferase activity of Clostridium difficile Toxin B is essential for disease pathogenesis.Clostridium difficile Toxin A Undergoes Clathrin-Independent, PACSIN2-Dependent EndocytosisRisk Factors and Outcomes for Bloodstream Infections Secondary to Clostridium difficile Infection.Bacterial probiotics as an aid in the control of Clostridium difficile disease in neonatal pigs.Cloning and variation of ground state intestinal stem cellsClostridium sordellii Lethal-Toxin Autoprocessing and Membrane Localization Activities Drive GTPase Glucosylation Profiles in Endothelial Cells.Predominance and high antibiotic resistance of the emerging Clostridium difficile genotypes NAPCR1 and NAP9 in a Costa Rican hospital over a 2-year period without outbreaksHigh mobility group box1 protein is involved in acute inflammation induced by Clostridium difficile toxin A.Clostridium difficile toxin B-induced necrosis is mediated by the host epithelial cell NADPH oxidase complex.Retrocyclins neutralize bacterial toxins by potentiating their unfolding.Vaccines against Clostridium difficile.Glucosyltransferase-dependent and -independent effects of TcdB on the proteome of HEp-2 cells.Investigation of the Cross-talk Mechanism in Caco-2 Cells during Clostridium difficile Infection through Genetic-and-Epigenetic Interspecies Networks: Big Data Mining and Genome-Wide Identification.Pathogenic effects of glucosyltransferase from Clostridium difficile toxins.Binding and entry of Clostridium difficile toxin B is mediated by multiple domains.Host response to Clostridium difficile infection: Diagnostics and detection.Pyknotic cell death induced by Clostridium difficile TcdB: chromatin condensation and nuclear blister are induced independently of the glucosyltransferase activity.A novel approach to generate a recombinant toxoid vaccine against Clostridium difficile.Clostridium difficile toxins A and B: Receptors, pores, and translocation into cells.Glucosyltransferase Activity of Clostridium difficile Toxin B Triggers Autophagy-mediated Cell Growth Arrest.Comment on "A small-molecule antivirulence agent for treating Clostridium difficile infection".A small-molecule antivirulence agent for treating Clostridium difficile infection.
P2860
Q26751477-9F25DBE4-6D6F-4C47-867B-512924F791E5Q26770068-15853779-516E-4CB8-BAB2-682D80D722FCQ26775010-F48F4769-1E5B-4BA6-B844-DC4EE26B10C4Q27026464-B91F13B1-3F16-43D2-B500-B34C94C69C02Q30276645-53A4F8B0-F98D-4BF0-A4C3-3BEA26B3A8A4Q30300865-445A6B07-DC51-44C6-8BC0-B70947C6BB2FQ30300885-BD82BE0F-ED38-43AF-955D-8ACFDA76EA91Q34026271-7E829BDC-2B80-4D9D-BCBC-6D5E774B8D4AQ34395494-11B46999-901C-417E-A914-AB8D6C50C40FQ34406643-9141B064-8486-4D29-9F15-D8131B34925AQ34727874-BA4174FE-3E72-4A7E-8354-21C60D2E2CCDQ34955649-DE1BA561-471B-467F-988C-EE734BB76919Q35172641-B82DDBE9-6214-410B-847E-78A106172372Q35535318-9662FDCC-659B-45DE-9F31-869014C29FDEQ35619086-F9B6BAD8-BA8E-4575-8656-C93242EBB4ECQ35677587-4DBCE24B-2A71-4131-B71E-F6E4D73441AEQ35699130-9B2EAF28-E4FC-4810-945E-E0DC0A74730DQ36148926-58C514D3-30C9-4972-8F50-0C4B3D0C0C09Q36189901-42CCEFCA-8FE6-45F5-97BF-26F78B203F47Q36220118-E45190EB-93CD-4D0C-82C2-50CEC3FC7633Q36439081-30D930EF-96FB-4CA9-A465-5C57799C0889Q36463014-36851BD8-1DBA-4620-A044-C4C8BC02A355Q36860891-A796C5DA-A24A-4E56-8021-F3F3C5250FEEQ36891374-2AF513D4-F2B5-496F-AF3C-0B895596D286Q36970016-AA4B8AD3-9B18-4070-AC53-01B354181734Q37020097-CE3F7F0F-A519-4F5E-A375-4E1835B2D71EQ37319468-2DC0C8D9-9761-4A95-942C-696B40720752Q37545884-5DC53BF8-CF2D-4A9F-8445-27C08B66DF85Q38196682-16CF9E81-2DD1-4DE1-97CC-2AF140B96B54Q38375614-FED6C291-9350-441E-9003-0B8200D73D45Q38616692-67D13463-0CAE-4ECE-86A3-61772CB05982Q38797967-FC239BD1-239D-414C-8D4D-E27DF435BBE5Q38817126-C705F218-1C98-4869-95B5-0B4DA7FB6C57Q38969987-44E6A53B-31F9-42B3-ACFE-8BC80D631511Q38988271-31D91090-1DD4-4E52-AB90-3EE7D2ECDE9AQ39158452-FA1DF36B-3236-46B6-9256-79F77C0EE2E6Q39330563-410C5F98-CBFE-46CE-8C6A-510F02172BF0Q40065545-7FBF6487-A352-4453-BCD4-92157C65FD28Q40399808-0F3D7136-1F0C-499C-802E-8002B0B639FAQ40984710-3943A366-62A9-4D6E-BDE5-08DD12A64CC3
P2860
Clostridium difficile Toxin B causes epithelial cell necrosis through an autoprocessing-independent mechanism
description
2012 nî lūn-bûn
@nan
2012 թուականին հրատարակուած գիտական յօդուած
@hyw
2012 թվականին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@ast
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@en
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@nl
type
label
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@ast
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@en
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@nl
prefLabel
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@ast
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@en
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@nl
P2093
P2860
P3181
P1433
P1476
Clostridium difficile Toxin B ...... ocessing-independent mechanism
@en
P2093
D Borden Lacy
David B Haslam
David Haslam
James R Goldenring
Jeffrey L Franklin
Lynne A Lapierre
Melissa A Farrow
Nicole M Chumbler
P2860
P304
P3181
P356
10.1371/JOURNAL.PPAT.1003072
P407
P577
2012-01-01T00:00:00Z