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AB93318

Anti-Clostridium difficile Toxin A antibody

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(1 Publication)

Rabbit Polyclonal Clostridium difficile Toxin A antibody. Suitable for ELISA and reacts with Clostridium difficile samples. Cited in 1 publication.

View Alternative Names

tcdA, toxA

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Clostridium difficile

Applications

ELISA

applications

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "ELISA" : {"fullname" : "ELISA", "shortname":"ELISA"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Clostridium difficile": { "ELISA-species-checked": "guaranteed", "ELISA-species-dilution-info": "", "ELISA-species-notes": "<p></p>" } } }

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein G
Storage buffer
pH: 7.2 Preservative: 0.09% Sodium azide Constituents: PBS
Shipped at conditions
Blue Ice
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Clostridium difficile Toxin A also known as C. diff toxin A or enterotoxin A acts mechanically by disrupting the cytoskeleton of intestinal epithelial cells. Weighing approximately 308 kDa this toxin gets expressed by Clostridium difficile bacteria during infection. C. diff toxin A enters the host cells inactivating Rho family GTPases leading to cell rounding and apoptosis. This disruption contributes to the weakening of the gut lining increasing its permeability.
Biological function summary

The main role of C. diff toxin A involves causing inflammation in the colonic mucosa. It functions as part of a dual toxin system with Toxin B. Toxin A binds to receptors on the surface of intestinal cells initiating a cascade that recruits neutrophils and other immune cells. This immune response exacerbates tissue damage and results in the observed symptoms of C. diff infections. The interaction with Toxin B enhances its pathogenic capacity further altering the tight junctions within the gut epithelium.

Pathways

C. diff toxin A affects the Rho-GTPase signaling pathway by acting as a glucosyltransferase and modifying small GTPases like Rho Rac and Cdc42. These changes impair the cell's cytoskeletal dynamics and disrupt cellular functions related to structural maintenance. Furthermore C. diff toxin A also influences the NF-kB pathway which plays a role in inflammation and immune responses. Toxin A's role in modifying these pathways highlights the coordinated interplay with Toxin B promoting inflammation and cytotoxicity.

The role of C. diff toxin A is prominent in Clostridium difficile infections (CDI) a significant cause of antibiotic-associated diarrhea and colitis. The presence of C. diff toxin A connects strongly to the severity of CDI leading to prolonged illness and complications like pseudomembranous colitis. Studies indicate an interaction with proteins like Toxin B that enhances the severity of infection and tissue destruction. Understanding C. diff toxin A's mechanisms can assist in developing therapeutic strategies targeting both toxins for effective treatment of CDI.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Publications (1)

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Frontiers in genetics 6:274 PubMed26379702

2015

Prolactin and growth hormone affect metaphase-II chromosomes in aging oocytes via cumulus cells using similar signaling pathways.

Applications

Unspecified application

Species

Unspecified reactive species

Irina Y Lebedeva,Galina N Singina,Alexander V Lopukhov,Ekaterina N Shedova,Natalia A Zinovieva
View all publications

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