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For pharmaceutical makers, the discovery of unique biological pathways, such as those found in the malaria parasite, suggests new drug targets. Theoretically, a drug that can interrupt such a pathway will have limited, if any, impact on circuits in human cells, reducing the likelihood of toxic side effects. Theoretically. In reality, pharmaceutical companies aren’t exactly tripping over themselves to make new drugs for malaria – a disease that strikes mainly in poor countries. But the general idea has great promise, says Ideker, who now plans to compare the interactomes of different HIV strains to see whether any chinks in that virus’s armor come to light.
George Church, who directs the Lipper Center for Computational Genetics at Harvard Medical School, has high respect for Ideker but adds another caveat: existing interactome data comes from fast, automated tests that simply aren’t that accurate yet. “The way I divide the omes is by asking, Are these data permanent, or are they going to be replaced by something better?” says Church. Data on the DNA sequences of genomes, Church says, is permanent. But interactome data? “There’s a 50-50 chance that this will be true or accepted in two years,” says Church. “That’s not Trey’s fault. He’s one of the people who is trying to make it more rigorous.”
Ideker agrees that “there’s a lot of noise in the system,” but he says the continuing flood of interactome data is making what happens inside different cells ever more clear. “Within five years, we hope to take these interaction data and build models of cellular circuitry to predict actions of drugs before they’re in human trials. That’s the billion-dollar application.”
James Collins – Synthetic gene networks
Bernhard Palsson – Metabolic networks
University of California, San Diego
Marc Vidal – Comparison of interactomes among species
Dana-Farber Cancer Institute, Boston, MA
Home page image courtesy of Gregg Segal.