Although studies of lynx1 and other members of this intriguing prototoxin protein family are still in the early stages, the researchers say they may help in understanding nicotine addiction or possibly human genetic diseases caused by defective prototoxins.
Howard Hughes Medical Institute investigatorNathaniel Heintz and his colleagues Ins Ibaez-Tallon and Julie Miwa at The Rockefeller University and colleagues at The Mayo Foundation and Columbia University reported in the March 14, 2002, issue of the journal Neuron that lynx1 is an interesting new modulator of nicotinic acetylcholine receptors.
Julie Miwa, a member of Heintzs laboratory and co-author of the Neuron article, first discovered lynx-1 in 1999. The discovery was especially intriguing, said Heintz, because it confirmed that mammals harbored a natural, or endogenous, protein resembling snake venom that could affect the nervous system. At the time the discovery was made, such an assumption was scientifically risky, said Heintz.
It was an appealing hypothesis that there might be an endogenous neurotoxin-like molecule that regulated some sort of receptor in the nervous system, said Heintz. But Julie was very, very brave to pursue this gene and its protein product on such a flimsy basis.
Miwas initial work showed that lynx1 was concentrated in the nervous system. Additional studies in collaboration with Ibaez-Tallon showed that lynx-1 altered the function of nicotinic acetylcholine receptors. Acetylcholine is a neurotransmitt
Contact: Jim Keeley
Howard Hughes Medical Institute