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Healing power in a gene

With age, the body deteriorates. Muscles atrophy. Bones grow thin. The skin loses its elasticity. Wounds are slow to heal. Our tissues don't regenerate the way they did in youth.

University of Illinois at Chicago researcher Robert Costa believes he knows why: our FoxM1B gene retires.

In a paper to be published in the Dec. 24 issue of the Proceedings of the National Academy of Sciences, Costa's research group has shown that the FoxM1B gene, found on human chromosome number 12, is critical for tissues to heal and replenish themselves.

If the gene is defective or just tired out (as in old age and rare genetic disorders causing premature aging), DNA can't duplicate itself, and cells can't divide and multiply the way they normally do. The result: a flood of activity in genes associated with aging.

Costa has been working on the FoxM1B gene since he discovered the whole family of Fox genes in 1993. Research has since shown that Fox family genes, found in animals from insects on up through mammals, are involved in the entire life cycle of a cell -- its proliferation, maturation and death.

Fox is short for Forkhead Box, a name referring to a mutation in the gene in the fruit fly that causes a duplication in the head structure.

One key finding came last year: Costa's research group was studying the FoxM1B gene in mice; in particular how it affects growth of the liver after a portion of the organ is removed. One of the few adult organs capable in mammals of completely regenerating itself, the liver is also the only organ that regenerates from fully mature cells. Others, like blood, form new tissue from immature cells.

The experiment showed that the liver grew back at a rate typical of young mice -- a discovery that led Costa to dub FoxM1B the "fountain-of-youth gene."

In the new study, Costa's team set out to understand how FoxM1B directs the busy molecular traffic inside a cell to make it proliferate. In
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Contact: Sharon Butler
sbutler@uic.edu
312-355-2522
University of Illinois at Chicago
24-Dec-2002


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