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The researchers say that keeping tuberin “off” led to a hyper-activation of mTORC1 which they show caused the fatal damage. Next, the researchers looked at hearts in mice that had tuberin “turned up.” Hearts from these mice also appeared wholesome, however after they have been careworn using the identical situations of elevated blood pressure, they remained wholesome. The hearts had been nonetheless regular in size and the mice stayed alive. Mice, like humans have a pair of each chromosome in every cell. Kass and crew reasoned that if both 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? In the subsequent experiments, the researchers looked at what would occur if mice had only one copy of the gene mutation that made tuberin behave as if it all the time had phosphates connected. In these experiments the hearts stayed normal in dimension and had good function regardless of excessive blood pressure stress, displaying only a single mutation was ample to guard the guts.

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