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Operating in Kass' laboratory, lead author and postdoctoral fellow Mark Ranek, Ph.D., was studying how this other protein referred to as Protein Kinase G, protected heart tissue from injury and condition. But as South Korean researchers explained, these products can develop into much less efficient in excess of time as the growth of tissue close to the metal device narrows the artery once more. Employing genetic engineering tools in heart muscle and connective tissue cells, the team mutated human tuberin protein in the precise areas that had been altered by protein kinase G. The alterations made the cells behave in a single of two methods: one type of mutation «turned up» the effect of tuberin all the time though the other fundamentally «turned down» its result all the time. In the cells with tuberin «turned down», nothing altered in the cells at rest.

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