Clostridium difficile (Toxin A) Antibody, IgG1, Clone: [253/422], Mouse, Monoclonal

Catalog Number: NBT-MSM1-202-P0
Article Name: Clostridium difficile (Toxin A) Antibody, IgG1, Clone: [253/422], Mouse, Monoclonal
Biozol Catalog Number: NBT-MSM1-202-P0
Supplier Catalog Number: MSM1-202-P0
Alternative Catalog Number: NBT-MSM1-202-P0-20,NBT-MSM1-202-P0-100
Manufacturer: NeoBiotechnologies
Host: Mouse
Category: Antikörper
Application: ELISA, IF
Species Reactivity: Bacteria
Immunogen: C. difficile Toxin A
Alternative Names: Clostridium difficile, C. difficile, tcdA, toxA
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.
Clonality: Monoclonal
Clone Designation: [253/422]
Molecular Weight: 308kDa (Toxin A)
Isotype: IgG1
NCBI: Not Applicable
UniProt: P16154
Form: 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.
Antibody Type: Monoclonal Antibody
Application Notes: ELISA (For coating use Ab at 1-5ug/ml, order Ab without BSA),Immunofluorescence (1-2ug/ml), Optimal dilution for a specific application should be determined.