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“Instead of turning mTORC1 off, we had something that looked more like a car brake, that was effective only if the car (mTORC1) was on and active,” says Ranek. Kass says the research team concluded that keeping tuberin “turned down” was like lifting the chemical foot off a brake pedal, triggering super-activity in mTORC1, while in the cells with tuberin “turned on”, the brake was pushed harder, and mTORC1 remained inactive despite the stimulating hormones. Like the many other proteins known to alter tuberin, Ranek found protein kinase G altered tuberin by adding phosphates to it, but in a previously unidentified region that turned out to provide the sought after brake-like effect. Working in Kass’ laboratory, lead author and postdoctoral fellow Mark Ranek, Ph.D., was studying how this other protein called Protein Kinase G, protected heart tissue from damage and disease Read through the mails and you will soon understand that it has nothing to do with commerce or business. In this case the email is successfully delivered and will be filtered out later.

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