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Clostridium difficile toxin B activates dual caspase-dependent and caspase-independent apoptosis in intoxicated cells.
TcdB from hypervirulent Clostridium difficile exhibits increased efficiency of autoprocessing.
Clostridium difficile 027/BI/NAP1 encodes a hypertoxic and antigenically variable form of TcdB.
Coordination between T helper cells, iNKT cells, and their follicular helper subsets in the humoral immune response against Clostridium difficile toxin B.
Clostridium difficile ClpP Homologues are Capable of Uncoupled Activity and Exhibit Different Levels of Susceptibility to Acyldepsipeptide Modulation.
Intrinsic Toxin-Derived Peptides Destabilize and Inactivate Clostridium difficile TcdB.
Determination of serum antibodies to Clostridium difficile toxin B in patients with inflammatory bowel disease.
Variations in TcdB activity and the hypervirulence of emerging strains of Clostridium difficile.
Clostridium difficile infection.
Memory B Cells Encode Neutralizing Antibody Specific for Toxin B from the Clostridium difficile Strains VPI 10463 and NAP1/BI/027 but with Superior Neutralization of VPI 10463 Toxin B.
Variations in virulence and molecular biology among emerging strains of Clostridium difficile.
Cell-penetrating peptides derived from Clostridium difficile TcdB2 and a related large clostridial toxin.
pH-induced conformational changes in Clostridium difficile toxin B.
Clostridium difficile toxins: mechanism of action and role in disease.
Mutational analysis of the enzymatic domain of Clostridium difficile toxin B reveals novel inhibitors of the wild-type toxin.
Identification of Clostridium difficile toxin B cardiotoxicity using a zebrafish embryo model of intoxication.
Characterization of a C. difficile Toxin-Encoded Cell Penetrating Peptide
Systemic events in Clostridium difficile associated disease