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Clostridium difficile Zoom

Clostridium difficile

anti-Clostridium difficile ToxinA mouse monoclonal, EBS-I-100, purified

EBS-I-100 reacts with C. difficile Toxin A, protein enterotoxin that is able to disrupt intestinal epithelial cells via its transferase activity and ability to monoglucosylate members of the Rho family.
Cat. No.: 691642
Quantity:  1 mL (100 µg/ml)
No. of experiments:  ≤ 2000 (IHC, 50 µl/slide)

Delivery Time: usually 5-10 working days

$425.00
Excl. 19% Tax, excl. Shipping Cost

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Specifications

Product description

Host mouse
Antibody Type monoclonal
Isotype IgG3 kappa
Clone EBS-I-100
Immunogen C. difficile toxin A
Purification affinity chromatography
Conjugate unconjugated
Formulation PBS with 0.02 % sodium azide
Storage store at 2-8°C
No. of experiments ≤ 2000 (IHC, 50 µl/slide)
Intended use Research use only
Tested species reactivity C. difficile (negative with V. cholera, P. aeruginosa)

Applications

Tested applications Tested dilutions
ELISA assay dependent
Immunocytochemistry (ICC)/ Immunofluorescence (IF) 1:100-1:200 (0.5-1.0 µg/ml)
Immunohistochemistry (IHC) - frozen 1:50-1:100 (1-2 µg/ml)

Background

Details

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.

Positive control: Clostridium difficile extract or infected cells or tissue.

Reference

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