Promotional price valid on web orders only. Your contract pricing may differ. Interested in signing up for a dedicated account number?
Learn More

C. botulinum BoNT-C1 Heavy Chain Mouse anti-Bacteria, Clone: 580223, Invitrogen™

Mouse Monoclonal Antibody

Manufacturer:  Invitrogen MA524261

Catalog No. PIMA524261


Add to cart

Description

Description

Reconstitute in sterile PBS to a final concentration of 0.5 mg/mL.

Botulinum neurotoxin type A is one of the seven serotypes of Botulinum Neurotoxins (BoNTs) produced by various strains of Clostridium botulinum. BoNTs are synthesized as inactive single chain protein precursors and activated by proteolytic cleavage to generate disulfide-linked two-chain proteins. The 50 kDa light chain contains the catalytic domain, whereas the 100 kDa heavy chain contains an internal translocation domain and a receptor binding domain. BoNTs are the most potent protein toxins for humans. As zinc proteases, they cleave SNARE proteins to elicit flaccid paralysis in botulism by blocking acetylcholine release at the neuromuscular junction. E. coli-expressed recombit light chains are active proteases. However, they are not toxic because they cannot enter into host cells in the absence of the heavy chains.
Specifications

Specifications

C. botulinum BoNT-C1 Heavy Chain
Monoclonal
0.5 mg/mL
PBS with 5% trehalose and No Preservative
BONTC1; Clostridium botulinum BoNT-C1
E. coli-derived recombit C. botulinum BoNT-C1 Heavy Chain Asn866-Glu1291
Protein A/G
RUO
Antibody
Monoclonal
Immunoprecipitation, Western Blot
580223
Unconjugated
Lyophilized
Mouse
IgG1
100 μg
-20° C, Avoid Freeze/Thaw Cycles
Primary
Bacteria
Documents
Provide Content Correction

We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.

Product Title

By clicking Submit, you acknowledge that you may be contacted by Fisher Scientific in regards to the feedback you have provided in this form. We will not share your information for any other purposes. All contact information provided shall also be maintained in accordance with our Privacy Policy.

Cancel Submit