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Corynebacterium diphtheriae 3-phage

Diphtheria toxin, an exotoxin of Corynebacterium diphtheriae infected with a specific lysogenic phage, catalyzes the ADP-ribosylation of EF-2 on the unique amino acid diphthamide in mammalian cells. This modification inactivates EF-2 and thereby specifically inhibits mammalian protein synthesis. Many animals (eg, mice) are resistant to diphtheria toxin. This resistance is due to inability of diphtheria toxin to cross the cell membrane rather than to insensitivity of mouse EF-2 to diphtheria toxin-catalyzed ADP-ribosylation by NAD. [Pg.372]

One of the primary killers of children prior to immunization was upper respiratory tract infections by Corynebacterium diphtheriae. Toxin produced by a lysogenic phage that is carried by some strains of this bacteria causes the lethal effects. It is lethal in small amounts because it blocks protein synthesis. The viral toxin is composed of two parts. The B portion binds a cell s surface and injects the A portion into the cytosol of cells. The A portion ADP-ribosylates a histidine-derived residue of the elongation factor 2 (EF-2) known as diphthamide. This action completely blocks the ability of EF-2 to translocate the growing polypeptide chain. [Pg.296]

Toxins capable of catalyzing such a reaction include diphtheria toxin, secreted by lysogenic strains of Corynebacterium diphtheriae carrying the phage-encoded toxin gene (DT), and the exotoxin A from Pseudomonas aeruginosa (ETA). Both catalyze the ADP-ribosylation of a posttranslationally-modified histidine residue (called diphthamide) in EF-2. [Pg.317]


See other pages where Corynebacterium diphtheriae 3-phage is mentioned: [Pg.62]    [Pg.114]    [Pg.752]    [Pg.2351]    [Pg.1236]    [Pg.584]    [Pg.2]    [Pg.2350]    [Pg.18]   
See also in sourсe #XX -- [ Pg.62 ]

See also in sourсe #XX -- [ Pg.67 ]




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Corynebacterium diphtheriae

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Phage

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