Clostridium difficile Toxin B, Recombinant

Clostridium difficile is the leading cause of hospital-acquired diarrhea, known as C. difficile-associated disease. The estimated number of cases of C. difficile-associated disease exceeds 250,000 per year (1), with health care costs approaching US $1 billion annually (2). \n\nThe major virulence factors produced by C. difficile are two toxins, TcdA and TcdB. Both toxins can monoglucosylate and inactivate Rho family small GTPases within target cells, leading to disruption of vital signaling pathways in the cell, subsequently causing diarrhea, inflammation, and damage of colonic mucosa (3,4,5). Both toxins have a similar tripartite structure comprised of an N-terminal glucosyltransferase domain, a C-terminal receptor binding domain, and a small hydrophobic span possibly involved in toxin translocation (6). \n\nOur recombinant TcdB consists of the enzymatic domain. Both TcdA and TcdB also have potassium-dependent UDPGlc hydrolase activity, which is essentially glucosyltransferase activity with water as the acceptor molecule (7). Under the same conditions, UDP-glucose hydrolysis by TcdB occurs at a rate about 5-fold greater than that of TcdA.\n\nSource: \nRecombinant corresponding to Met1-Leu543 from C. difficile Toxin B/TcdB, C-terminal 6-His tag, expressed in E. coli, Accession # P18177.\n\nN-Terminal Sequence Analysis:\nSer2\n\nBiological Activity:\nMeasured by its ability to hydrolyze UDP

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SPECIFICATIONS

Catalog Number

C5856-02

Size

20ug

Form

Supplied as a liquid in 25mM Tris base, 150mM sodium chloride, pH 7.5.

Purity

~95% (SDS-PAGE shows a band between 60-65kD under reducing conditions.) Endotoxin: <1EU/ug (LAL)

References

1. Wilkins, T.D. and Lyerly, D.M., J. Clin. Microbiol 41: 53 (2003). 2. Kyne, L., et al., Clin. Infect. Dis. 34: 346 (2002). 3. Voth, D.E. and Ballard, J.D., Clin. Microbiol. Rev. 18: 247 (2005). 4. Chaves-Olarte, E., et al., J. Biol. Chem. 271: 6925 (1996). 5. Just, I., et al., J. Biol. Chem. 270: 13,932 (1995). 6. Hammond, G.A. and Johnson, J.L., Microb. Pathog. 19: 203 (1995). 7. Ciesla, W.P. Jr. and Bobak, D.A., J. Biol. Chem. 273: 16,021 (1998).