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Kass says the research staff concluded that conserving tuberin "turned down" was like lifting the chemical foot off a brake pedal, triggering super-activity in mTORC1, whereas within the cells with tuberin "turned on", the brake was pushed tougher, and mTORC1 remained inactive regardless of the stimulating hormones.
But the drug seems to increase ranges of a chemical referred to as GMP, which is known to affect the intestinal lining, the researchers stated. When the researchers seemed at the cells that had tuberin "turned up", they noticed no modifications in the cells when the identical hormones were added.
Kass and workforce reasoned that if each copies of the tuberin gene mutated to "turned up" resulted in regular hearts, what would happen if only one copy of the gene was mutated? "We had been struck by how potent the effect was, as just one copy of the gene mutation was wanted to get the total protective effect," says Ranek.