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Clostridium enterotoxin

InterPro Family

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General referenceInterpretive dossier study · Crown Archives visual atlas
Record originEnglish Wikipedia
Text licenseCC BY-SA 4.0
Source revisionSep 27, 2025
Entity authorityQ24724496 ↗
Source-derived summary

Clostridium enterotoxins are toxins produced by Clostridium species. Clostridial species are one of the major causes of food poisoning/gastrointestinal illnesses. They are anaerobic, gram-positive, spore-forming rods that occur naturally in the soil. Among the family are: Clostridium botulinum, which produces one of the most potent toxins in existence; Clostridium tetani, causative agent of tetanus; and Clostridium perfringens, commonly found in wound infections and diarrhea cases.

The major virulence factor of C. perfringens is the CPE enterotoxin, which is secreted upon invasion of the host gut, and contributes to food poisoning and other gastrointestinal illnesses. It has a molecular weight of 35.3 kDa, and is responsible for the disintegration of tight junctions between epithelial cells in the gut. This mechanism is mediated by host claudin-3 and claudin-4 receptors, situated at the tight junctions.

Clostridium enterotoxin is a nine-stranded beta sheet sandwich in shape. It has been determined that it is very similar to other spore-forming bacteria. The binding site is between beta sheets eight and nine.

Editorial summary

This brief starts where responsible research should: with the source description of “Clostridium enterotoxin” as interPro Family. Everything that follows is an evidence route, not borrowed authority.

Editorial reviewA dependable orientation record for establishing vocabulary, names and a first evidence trail. The current 165-word lead offers orientation but no explicit four-digit date, so chronology should not be assumed. The selected authority fields contribute no independent date. The account is most persuasive where Clostridium, enterotoxin and InterPro can be independently traced.
Editorial analysis

Why this record matters

The subject matters to the general reference register because the source frames it as interPro Family. Its deeper value depends on whether names, dates, institutions and citations support that framing.

Evidence profile

Named sources, stable identifiers and responsible institutions provide the strongest route from overview to verifiable evidence. The source revision retrieved here is dated Sep 27, 2025. The linked authority identifier is Q24724496. None of the 0 selected statements returned an explicit reference.

Critical limits

Overview language is designed for orientation and should not be treated as a substitute for the evidence cited beneath it. The lead is largely declarative, so disagreement and counter-evidence require a deliberate search beyond the opening account. Authority statements aid reconciliation but still require their own references, qualifiers and ranks to be checked.

How to read it

Use the entry as an orientation point, then follow its citations and revision history. Names, dates and institutional relationships should be checked against the original record.

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The closest primary source, responsible institution and strongest cited specialist reference.

Three-step research path

  1. Establish the record: confirm the title “Clostridium enterotoxin”, its source revision and the description used here.
  2. Expand the search: follow Clostridium enterotoxin primary sources, Clostridium enterotoxin archive and Clostridium research across catalogues and specialist indexes.
  3. Test the account: compare the strongest cited source with the responsible institution’s current record and note any disagreement.

Questions for further research

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Source & attribution

This entry incorporates text from “Clostridium enterotoxin” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.