Clostridium perfringens enterotoxin acts by producing small molecule permeability alterations in plasma membranes.
Clostridium perfringens enterotoxin (CPE) appears to utilize a unique mechanism of action to directly affect the plasma membrane permeability of mammalian cells. CPE action involves a multi-step action which culminates in cytotoxicity. Initially CPE binds to a protein receptor on mammalian plasma membranes. The membrane-bound CPE then becomes progressively more resistant to release by proteases (a phenomenon consistent with the insertion of CPE into membranes). This 'inserted' CPE then participates in the formation of a large complex in plasma membranes which contains one CPE: one 70 kDa membrane protein: one 50 kDa membrane protein. Upon formation of large complex, plasma membranes become freely permeable to small molecules such as ions and amino acids. This CPE-induced disruption of the cellular colloid-osmotic equilibrium then causes secondary cellular effects and cell death.
McClane
B A
BA
Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, PA 15261.
D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D002462:Cell Membrane / Q000187:drug effects*; D002463:Cell Membrane Permeability / Q000187:drug effects; D003016:Clostridium perfringens / Q000737:chemistry / Q000472:pathogenicity*; D004768:Enterotoxins / Q000737:chemistry / Q000633:toxicity*; D006801:Humans; D008969:Molecular Sequence Data; D008970:Molecular Weight
D004768:Enterotoxins