Diptheria Toxin, CRM Mutant, also known as CRM197, does not have NAD:EF2 ADP-ribosyltransferase activity due to an amino acid substitution of glycine to glutamic acid, that results in the alteration of the NAD+ binding site, in fragment A. The non-toxic diptheria toxin, CRM197, can inhibit bladder smooth muscle cell proliferation through its interaction with HB-EGF. Research shows that CRM197 does not catalyze ADP ribosylation of elongation factor-2 (EF-2), and failed to induce apoptosis in Vero cells in the presence of brefeldin and okadaic acid (sc-3513). Both the mutant CRM197 and the wild type diptheria toxin are alike immunologically.
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PMID: # 6427753 Giannini, G. et al. 1984. Nucleic Acids Res. 12: 4063-4069.