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Clostridium difficile (Toxin A) Antibody [253/422]

In Stock
Catalog Number Formulation Size Price
Purified Ab with BSA and Azide at 200ug/ml
Purified Ab with BSA and Azide at 200ug/ml
Purified Ab WITHOUT BSA and Azide at 1.0mg/ml
Flat Rate Domestic: $60 | Orders outside the US - Contact Us for Order Information | Ships next business day

Applications & Dilutions

Applications Tested Dillution Protocol Note
Immunofluorescence (IF)


This MAb reacts with C. difficile Toxin A, but not with Cholera subunit a, Cholera toxin, Pseudomonas aeruginosa exotoxin A, H-LT, P-LT. Clostridium difficile is a major nosocomial pathogen that causes antibiotic- associated colitis. Clostridium difficile 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. Clostridium difficile Toxin A is a toxin that is composed of 39 repeats that are responsible for binding to intestinal epithelial cell surface carbohydrates. Clostridium 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.

Product Properties & Targets

Antibody Type
Species Reactivity
Isotype / Light Chain
IgG1 / Kappa
Cellular Localization
Host cell membrane, Host cytoplasm, Host cytosol, Host endosome membrane, Secreted
Gene Name
Positive Control
Clostridium difficile extract or infected cells. Tissue.
C. difficile Toxin A
Alternate Names
Toxin A, Clostridium difficile; C. difficile; tcdA; toxA

Database Links

Entrez Gene ID

Additional Information

Chromosome Location
Not Applicable
Mol. Weight of Antigen
308kDa (Toxin A)


  • Precursor of a cytotoxin that targets and disrupts the colonic epithelium, inducing the host inflammatory and innate immune responses and resulting in diarrhea and pseudomembranous colitis (PubMed:20844489). TcdA and TcdB constitute the main toxins that mediate the pathology of C.difficile infection, an opportunistic pathogen that colonizes the colon when the normal gut microbiome is disrupted (PubMed:19252482, PubMed:20844489). Compared to TcdB, TcdA is less virulent and less important for inducing the host inflammatory and innate immune responses (PubMed:19252482). This form constitutes the precursor of the toxin: it enters into host cells and mediates autoprocessing to release the active toxin (Glucosyltransferase TcdA) into the host cytosol (By similarity). Targets colonic epithelia by binding to some receptor, and enters host cells via clathrin-mediated endocytosis (By similarity). Binding to LDLR, as well as carbohydrates and sulfated glycosaminoglycans on host cell surface contribute to entry into cells (PubMed:1670930, PubMed:31160825, PubMed:16622409). In contrast to TcdB, Frizzled receptors FZD1, FZD2 and FZD7 do not act as host receptors in the colonic epithelium for TcdA (PubMed:27680706). Once entered into host cells, acidification in the endosome promotes the membrane insertion of the translocation region and formation of a pore, leading to translocation of the GT44 and peptidase C80 domains across the endosomal membrane (By similarity). This activates the peptidase C80 domain and autocatalytic processing, releasing the N-terminal part (Glucosyltransferase TcdA), which constitutes the active part of the toxin, in the cytosol (PubMed:17334356, PubMed:19553670, PubMed:27571750).
  • Active form of the toxin, which is released into the host cytosol following autoprocessing and inactivates small GTPases (PubMed:7775453, PubMed:24905543, PubMed:30622517, PubMed:22747490, PubMed:22267739). Acts by mediating monoglucosylation of small GTPases of the Rho family (Rac1, RhoA, RhoB, RhoC, Rap2A and Cdc42) in host cells at the conserved threonine residue located in the switch I region ('Thr-37/35'), using UDP-alpha-D-glucose as the sugar donor (PubMed:7775453, PubMed:24905543, PubMed:30622517, PubMed:22747490, PubMed:22267739). Monoglucosylation of host small GTPases completely prevents the recognition of the downstream effector, blocking the GTPases in their inactive form, leading to actin cytoskeleton disruption and cell death, resulting in the loss of colonic epithelial barrier function (PubMed:7775453). Also able to catalyze monoglucosylation of some members of the Ras family (H-Ras/HRAS, K-Ras/KRAS and N-Ras/NRAS), but with much less efficiency than with Rho proteins, suggesting that it does not act on Ras proteins in vivo (PubMed:30622517).

Key References

  • Kim, H., et al. 2005. Gastroenterology 129: 1875-1888.

Storage & Stability

Antibody with azide - store at 2 to 8°C. Antibody without azide - store at -20 to -80°C. Antibody is stable for 24 months. Non-hazardous. No MSDS required.


This antibody is available for research use only and is not approved for use in diagnosis.

Supplied as

200ug/ml of Ab Purified from Bioreactor Concentrate by Protein A/G. Prepared in 10mM PBS with 0.05% BSA & 0.05% azide. Also available WITHOUT BSA & azide at 1.0mg/ml.


There are no warranties, expressed or implied, which extend beyond this description. Company is not liable for any personal injury or economic loss resulting from this product.


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