[LMB] Real Life Bujold Science

[The Sundance Kid]

Howard Hughes Medical Institute researchers at Stanford University   
say they have increased bone mass in mice by tweaking a regulatory   
protein. Dr. Gerald Crabtree and pre-doctoral fellow Monte   
Winslow report slightly increasing the activity of a protein   
called NFATc1 causes massive bone accumulation, suggesting   
NFATc1 or other proteins that regulate its activity will make   
good targets for drugs to treat osteoporosis.  In vertebrates,   
bone is constantly being formed and broken down throughout life.   
Cells called osteoclasts continuously degrade bone, while cells   
called osteoblasts replenish it. "Ideally, they are perfectly   
balanced," said Crabtree, the senior author of the study. "Over   
the course of a lifetime, if everything goes well, we'll maintain   
almost exactly identical bone mass."  But if the balance is   
upset, and more bone is destroyed than formed, osteoporosis   
results, increasing the risk of fractures. "If you could find a   
small molecule that would flip 10 percent of the existing NFATc   
into the active form, you could favor the formation of osteoblasts   
and make stronger bones," said Crabtree. The research is reported   
in the journal Developmental Cell.   


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