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Cholera toxin mechanism. Cholera toxin (also known as choleragen and sometimes abbreviated to CTX, Ctx or CT) is an AB5 multimeric protein complex secreted by the bacterium Vibrio cholerae. [1] [2] CTX is responsible for the massive, watery diarrhea characteristic of cholera infection. [3] It is a member of the heat-labile enterotoxin family.
Sambhu Nath De isolated the cholera toxin and demonstrated the toxin as the cause of cholera in 1959. The bacterium has a flagellum (a tail like structure) at one pole and several pili throughout its cell surface. It undergoes respiratory and fermentative metabolism.
These toxins consist of an AB5 multimer structure, in which a pentamer of B chains has a membrane-binding function and an A chain is needed for enzymatic activity. [3] The B subunits are arranged as a doughnut-shaped pentamer, each subunit participating in ~30 hydrogen bonds and 6 salt bridges with its two neighbours.
The secreted toxin attaches to the surface of the host mucosa cell by binding to GM1 gangliosides. GM1 consists of a sialic acid-containing oligosaccharide covalently attached to a ceramide lipid. The A1 subunit of this toxin will gain entry to intestinal epithelial cells with the assistance of the B subunit via the GM1 ganglioside receptor.
The toxin shares its mechanism with cholera toxin. [5] ArtAB toxin of Salmonella enterica has components similar to those found in two different families: the ArtA subunit is homologous with pertussis toxin A, while the ArtB subunit is homologous with subB as well as proteins found in other Salmonella strains. Under the categorize-by-A rule, it ...
Cholera toxin is an AB toxin that has five B subunints and one A subunit. The toxin acts by the following mechanism: First, the B subunit ring of the cholera toxin binds to GM1 gangliosides on the surface of target cells. If a cell lacks GM1 the toxin most likely binds to other types of glycans, such as Lewis Y and Lewis X, attached to proteins ...
The snail releases the toxin by absorbing water into the muscle cavity and it is released when the snail is attacked. [26] Once a human consumes the toxin, the individual could experience mild symptoms such as paresthesias of the lips or tongue, vomiting and headaches. The individual could also experience severe symptoms such as respiratory or ...
The first of these is accessory cholera enterotoxin (Ace). Ace is currently thought to be a minor coat protein of virion stage CTXφ, though the process by which the toxin could be released from the protein coat has not yet been identified. The second non-CT toxin encoded within the CTXφ genome is zonula occludens toxin (Zot). Zot, though ...