Native Clostridium difficile Toxoid B protein
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Native Clostridium difficile Toxoid B protein is a Clostridium difficile Full Length protein, expressed in Native, with >95%, suitable for SDS-PAGE, ELISA.
View Alternative Names
toxB, tcdB, Toxin B
- SDS-PAGE
Unknown
SDS-PAGE - Native Clostridium difficile Toxoid B protein (AB124002)
SDS-PAGE showing ab124002 at 270kDa.
Reactivity data
Product details
Antigenicity: Maintained to be no less than 90% of original toxin strength as measured by direct ELISA.
This protein is derived from a pathogenic organism, and may be involved in a disease process, consequently exposure may have adverse health effects.
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
TcdB acts as an important virulence factor of Clostridioides difficile infection contributing to the disease's pathogenesis by causing extensive intestinal damage. The toxin is not part of a multi-protein complex; it independently enters host cells using receptor-mediated endocytosis. Once inside it modifies important small GTPases that regulate the cytoskeleton leading to epithelial barrier dysfunction. The rapid cell damage caused by TcdB promotes inflammation and sets the stage for the onset of symptoms associated with Clostridioides difficile infections such as diarrhea and pseudomembranous colitis.
Pathways
TcdB significantly impacts signaling pathways that control the cytoskeleton and cellular adhesion. Its glucosylation of Rho family GTPases inactivates them effectively disrupting the Rho/Rock signaling pathway pivotal for maintaining cytoskeletal structure. This alteration compromises intercellular junctions and increases intestinal permeability. Additionally TcdB interacts with Rac1 and CDC42 further contributing to disruption in cell cycle regulation and immune response modulation within the gut epithelium.
Specifications
Form
Lyophilized
General info
Function
Toxin B. 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, PubMed : 24919149). TcdB constitutes the main toxin that mediates 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 TcdA, TcdB is more virulent and more important for inducing the host inflammatory and innate immune responses (PubMed : 19252482, PubMed : 24919149). This form constitutes the precursor of the toxin : it enters into host cells and mediates autoprocessing to release the active toxin (Glucosyltransferase TcdB) into the host cytosol (PubMed : 10768933, PubMed : 11152463, PubMed : 12941936, PubMed : 17334356, PubMed : 20498856). Targets colonic epithelia by binding to the frizzled receptors FZD1, FZD2 and FZD7, and enters host cells via clathrin-mediated endocytosis (PubMed : 27680706). Frizzled receptors constitute the major host receptors in the colonic epithelium, but other receptors, such as CSPG4 or NECTIN3/PVRL3, have been identified (PubMed : 25547119, PubMed : 26038560, PubMed : 27680706). Binding to carbohydrates and sulfated glycosaminoglycans on host cell surface also contribute to entry into cells (By similarity). 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 (PubMed : 11152463, PubMed : 12941936, PubMed : 24567384). This activates the peptidase C80 domain and autocatalytic processing, releasing the N-terminal part (Glucosyltransferase TcdB), which constitutes the active part of the toxin, in the cytosol (PubMed : 17334356, PubMed : 27571750).. Glucosyltransferase TcdB. Active form of the toxin, which is released into the host cytosol following autoprocessing and inactivates small GTPases (PubMed : 16157585, PubMed : 17901056, PubMed : 24905543, PubMed : 24919149, PubMed : 7777059, PubMed : 8144660). Acts by mediating monoglucosylation of small GTPases of the Rho family (Rac1, RhoA, RhoB, RhoC, RhoG 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 : 16157585, PubMed : 17901056, PubMed : 24905543, PubMed : 24919149, PubMed : 7777059). 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 : 24919149, PubMed : 7777059).
Sequence similarities
Belongs to the clostridial glucosylating toxin (LCGT) family.
Post-translational modifications
Toxin B. Undergoes autocatalytic cleavage to release the N-terminal part (Glucosyltransferase TcdB), which constitutes the active part of the toxin, in the host cytosol (PubMed:12941936, PubMed:17334356, PubMed:27571750). 1D-myo-inositol hexakisphosphate-binding (InsP6) activates the peptidase C80 domain and promotes autoprocessing (PubMed:17334356).
Subcellular localisation
Host endosome membrane
Target data
Product promise
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