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The alterations made the cells behave in one of two ways: one type of mutation “turned up” the effect of tuberin all the time while the other essentially “turned down” its effect all the time. But the complete shut-down of mTORC1 has its downside as it does so many things in normal cells, limiting prospects for using protein blockers as broader disease therapies, researchers say. But, when the researchers treated the cells with hormones that encourage them to grow, mTORC1 was super-activated and the cells enlarged more than the cells with normal tuberin.
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