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Clostridium perfringens cell surface receptor

Molecular classification
Receptor, Other
01

Overview

The term "Clostridium perfringens cell surface receptors" does not refer to a single, specific molecule, but rather to several different cell surface receptors utilized by various toxins produced by Clostridium perfringens to gain entry into host cells. For example: - The **iota toxin** binds its B subunit (Ib) to an as-yet-uncharacterized cell surface receptor to facilitate entry and translocation of the enzymatic subunit (Ia), which ADP-ribosylates actin and disrupts the cytoskeleton, resulting in cell rounding and death[1][3]. The exact molecular identity of this cell surface receptor remains uncharacterized. - The **enterotoxin** (CpE) from C. perfringens specifically targets **claudin-3 and claudin-4** proteins on epithelial cells as functional receptors, leading to cytotoxicity and gastrointestinal disease[4]. - Other toxins (such as TcdA, TcdB, TpeL) may use additional protein receptors, including LDL-receptor-related protein-1 (LRP1), chondroitin sulfate proteoglycan 4 (CSPG4), poliovirus receptor-like 3 (PVRL3), and members of the Frizzled receptor family, but these are primarily associated with Clostridioides (formerly Clostridium) difficile and not classic C. perfringens strains[2]. Because multiple, structurally diverse receptors are involved and many have not yet been definitively identified for all C. perfringens toxins, the term is not a precise molecular entity and should not be treated as a canonical single target.

Other names
Clostridium perfringens toxin receptorC. perfringens toxin cell entry receptor
02

Mechanism of action

Mediates binding and entry of C. perfringens toxins (e.g., iota toxin, enterotoxin) by serving as the cellular docking site for the toxin's binding component[1][3][4]

03

Biological functions

Cell entryToxin internalizationCell death
04

Disease associations

InfectionOther
05

Safety considerations

Ubiquity of receptor(s) may affect non-target tissuesOff-target toxicity with therapeutics that mimic toxins[4]

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