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Posted on Jul 28, 2005, 9 a.m.
By Bill Freeman
A gene previously linked to longevity has been found to suppress the ability of cells to divide. The finding, by Howard Hughes Medical Institute researchers, provides insight into how the gene, SIRT1, affects longevity.
A gene previously linked to longevity has been found to suppress the ability of cells to divide.
The finding, by Howard Hughes Medical Institute researchers, provides insight into how the gene, SIRT1 , affects longevity.
The researchers began studying SIRT1 because they were interested in how reports from other research groups suggested that the yeast version of the gene, Sir2 , extends the ability of cells to replicate.
There is speculation that influencing SIRT1 activity in human cells could affect longevity, and pharmaceutical companies are researching drugs that have such effects.
Publishing in the journal Cell Metabolism ( read abstract ), researchers led by Frederick W. Alt of Children's Hospital Boston and Harvard Medical School report suppressing SIRT1 in mouse embryonic fibroblasts.
"We had been studying SIRT1-knockout mice, which have a number of defects," says Alt . "And when we grew embryonic fibroblasts from those mice in culture, we observed that, unlike wild-type cells that only undergo a limited number of divisions before they reach senescence, SIRT1-deficient cells continued to grow on and on very well. That was quite surprising, because the findings in yeast and other lower organisms led those in field to speculate that if you got rid of mammalian SIRT1, the cells would senesce sooner. But in fact we got the opposite result; the cells survived and didn't undergo senescence."
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The finding, by Howard Hughes Medical Institute researchers, provides insight into how the gene, SIRT1 , affects longevity.
The researchers began studying SIRT1 because they were interested in how reports from other research groups suggested that the yeast version of the gene, Sir2 , extends the ability of cells to replicate.
There is speculation that influencing SIRT1 activity in human cells could affect longevity, and pharmaceutical companies are researching drugs that have such effects.
Publishing in the journal Cell Metabolism ( read abstract ), researchers led by Frederick W. Alt of Children's Hospital Boston and Harvard Medical School report suppressing SIRT1 in mouse embryonic fibroblasts.
"We had been studying SIRT1-knockout mice, which have a number of defects," says Alt . "And when we grew embryonic fibroblasts from those mice in culture, we observed that, unlike wild-type cells that only undergo a limited number of divisions before they reach senescence, SIRT1-deficient cells continued to grow on and on very well. That was quite surprising, because the findings in yeast and other lower organisms led those in field to speculate that if you got rid of mammalian SIRT1, the cells would senesce sooner. But in fact we got the opposite result; the cells survived and didn't undergo senescence."
Read Full Story
