The team also included researchers from the University of Houston; Ecole Supérieure de Biotechnologie Strasbourg, Illkirch, France; and Laval University, Quebec.
This study was supported from a grant from the National Institutes of Health.
PARP-1 is best known as a normal part of the cellular machinery that repairs damaged DNA.
But in certain types of cancer this enzyme actually enhances tumor survival and undermines chemotherapies designed to damage DNA in cancer cells.
A recent human clinical trial found that drugs that inhibited PARP-1 reduced tumor growth in breast-cancer patients with mutations in certain DNA-repair (BRCA-1 and BRCA-2) genes.
Other bacterial toxins, including cholera toxin and diphtheria toxin "ADP-ribosylate" host proteins in ways that enhance the survival or transmission of the bacteria that produce them.
"We were very excited about this finding, which we published in 2006," Blanke said.