Anti-Clostridium difficile Toxin A antibody [EBS-I-100] (STJ16101048)

SPECIFICATIONS
ClonalityMonoclonal
HostMouse
ConjugationUnconjugated
IsotypeIgG3k
ImmunogenA BALB/c mouse was immunized with C. difficile toxin A. Fusion partner: Sp2/0.
STJ16101048
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General Information

Short DescriptionMouse monoclonal anti-Clostridium difficile Toxin A for use in ELISA, IF and IHC in C.Difficile samples. Datasheet included with dilution recommendations, and related reagents.
ApplicationsELISA/IF/IHC
HostMouse
ReactivityC.Difficile
NoteSTRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.

Product Properties

ClonalityMonoclonal
Clone IDEBS-I-100
IsotypeIgG3k
ConjugationUnconjugated
ConcentrationCan be provided as 100 ยตg/mL, 500 ยตg/mL or 1mg/mL.
PurificationAffinity purified from tissue culture.
Dilution RangeELISA (solid phase: not known; tracer: 0, 001-100 ยตg/ml for 30 min at RT). Immunofluorescence (0.5-1 ยตg/ml). Immunohistology (1-2 ยตg/ml for 30 min at RT; an appropriate antigen retrieval method for staining of formalin-fixed tissues has not been esta
FormulationPBS with 0.02% Sodium Azide.
Storage InstructionStore for up to 1 year at 2-8ยฐC upon receipt.

Target Information

ImmunogenA BALB/c mouse was immunized with C. difficile toxin A. Fusion partner: Sp2/0.

Additional Info

Background EBS-I-100 reacts with C. difficile Toxin A, but not with V. cholerae subunit a, V. cholerae toxin, Pseudomonas aeruginosa exotoxin A, H-LT, P-LT. C. difficile is a major nosocomial pathogen that causes antibiotic-associated colitis and mediates inflammatory diarrhea by releasing two large protein enterotoxins (toxin A and toxin B) that are able to disrupt intestinal epithelial cells via their transferase activity and ability to monoglucosylate members of the Rho family. C. difficile toxin A is a toxin that is composed of 39 repeats that are responsible for binding to intestinal epithelial cell surface carbohydrates. C. difficile toxin A causes significant apoptosis of colonocytes which contributes to the formation of ulcers and pseudo-membranes in a pathway that involves p38-dependent activation of p53 and induction of p21, leading to cytochrome c release and caspase-3 activation through Bak activation.

Information sourced from Uniprot.org

Citations

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