Anti-Clostridium difficile Toxin B antibody [EPR23357-19],Abcam,AB270452

Patented technology Our RabMAb ® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb ® patents . What are the advantages of a recombinant monoclonal antibody? This product is a recombinant monoclonal antibody, which offers several advantages including: - High batch-to-batch consistency and reproducibility - Improved sensitivity and specificity - Long-term security of supply - Animal-free batch production For more information, read more on recombinant antibodies .

Host

Rabbit

Reactivity

Clostridium difficile

Application

WB

Platform ID

BAB577423377

Abcam

Headquarters

Discovery Drive Cambridge Biomedical Campus Cambridge CB2 0AX UK

Contact

Tel: +44 (0)1223 696000
Fax: +44 (0)1223 215 215

Product Specifications
Scientific Background

Specifications

NameAnti-Clostridium difficile Toxin B antibody [EPR23357-19]
Cat. No.AB270452
HostRabbit
IsotypeIgG
ReactivityClostridium difficile
ApplicationWB
ClonalityMonoclonal
Clone NumberEPR23357-19
Concentration0.513 mg/mL Batch dependent concentration
ImmunogenThe exact immunogen used to generate this antibody is proprietary information.
PurityAffinity purification Protein A
Appearance/FormLiquid
ShippingBlue Ice
FormulationpH: 7.2 - 7.4 Preservative: 0.05% Sodium azide Constituents: PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
Storage-20°C
Regulatory StatusResearch Use Only

Scientific Background

Target data 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). See full target information tcdB

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