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Systemically blocking the mechanistic target of rapamycin (mTOR) protein with an immunosuppressant drug has been shown to increase longevity in mice. Taking a new approach, researchers show in Cell Reports today (August 29) that cutting down the levels of mTOR through a genetic alteration also extends mouse lifespan, and delays the appearance of biomarkers of aging. “It’s clear that in many different model organisms, either pharmacologically or genetically, perturbations of this pathway extend lifespan,” said David Sabatini, a member of the Whitehead Institute for Biomedical Research in Cambridge, Mass., who was not involved in the study.
MTOR is a kinase involved in myriad cellular processes, from autophagy to protein synthesis. Genetic studies of TOR in other organisms, such as yeast and flies, have implicated a role for the enzyme in lifespan. In mammals, however, mTOR is required for survival, making a knockout mouse model unfeasible. So the National Heart, Lung and Blood Institute’s Toren Finkel and his colleagues decided to use a mouse in which transcription was only partially disrupted, reducing the levels of mTOR to about 25 percent of the normal amount.
Source: Here
MTOR is a kinase involved in myriad cellular processes, from autophagy to protein synthesis. Genetic studies of TOR in other organisms, such as yeast and flies, have implicated a role for the enzyme in lifespan. In mammals, however, mTOR is required for survival, making a knockout mouse model unfeasible. So the National Heart, Lung and Blood Institute’s Toren Finkel and his colleagues decided to use a mouse in which transcription was only partially disrupted, reducing the levels of mTOR to about 25 percent of the normal amount.
Source: Here
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