ArsB. ArsB creates the channel through which the arsenic is transported out of the cell, while ArsA forces the arsenic into the channel. Using crystallization and X-ray diffraction techniques, Dr. Gatti hopes to determine the mechanism behind the pump. Humans have significant resistance to arsenic, and it's clearly advantageous, because it's one of the few known inorganic carcinogens and is present in high concentrations in water in many places in Michigan. Arsenic can, however, become deadly if the intake of the carcinogen exceeds the pumping ability of the cellular system. A structurally similar system works in tumor cells, he said.
Cells normally have very small amounts of the proteins that extrude anti-tumor agents.
In tumor cells, these proteins become more abundant by virtue of a process of gene amplification. The cells become resistant to greater and greater amounts of anti-tumor drugs, and eventually the dosage cannot outrun the resistance without causing toxic side effects to the patient. He predicts that when these cases are studied in detail it will be found that amplification of the genes encoding the human arsenic pump is responsible for the emergence of the resistance. If we understand the mechanism, we can possibly develop inhibitors for the pumps and reverse the resistance.