Reuben Shaw wanted nothing more than to study tumor suppressor genes, but his results took him on another path. "As fate has it," he sighs in mock defeat, "diabetes will be a part of my research from here on out."
In 1993 Shaw joined Tyler Jacks' laboratory at the Massachusetts Institute of Technology as a graduate student. Jacks' lab studied a number of tumor suppressors, including p53 and retinoblastoma. The latest to be cloned, neurofibromatosis type II (Nf2), held certain appeal. From its sequence, Nf2 looks like a cytoskeletal protein, not a molecule that would be related to cell growth. "It was a complete enigma," Shaw says. Shaw determined that the Nf2 gene's protein, called merlin, is part of the signaling pathway downstream of the GTPase Rac, which coincidentally he had studied as an undergrad. It was "one of the twists of scientific fate," he says....
Title: Assistant Professor at the Salk Institute for Biological Studies
1. R.J. Shaw et al., "The tumor suppressor LKB1 kinase directly activates AMP-activated kinase and regulates apoptosis in response to energy stress," Proc Natl Acad Sci, 101:3329-35, 2004. (Cited in 157 papers) 2. R.J. Shaw et al., "The LKB1 tumor suppressor negatively regulates mTOR signaling," Cancer Cell, 6:91-9, 2004. (Cited in 118 papers) 3. R.J. Shaw et al., "The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin," Science, 310:1642-6, 2005. (Cited in 52 papers)