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Among the most studied protein machines in history, mTORC1 has long been known to sense whether a cell has enough energy to build the proteins it needs to multiply as part of growth. Because faulty versions of mTORC1 contribute to the abnormal growth seen in cancer, drugs targeting the complex have been the subject of 1,300 clinical trials since 1970.
Now a new study finds that mTORC1 has a second function of profound importance: controlling how "crowded" human cells become.
Researchers - NYU - School - Medicine - Online
Led by researchers at NYU School of Medicine and published online in the journal Cell on June 21, the finding explains for the first time the workings of a physical quality that cells use to regulate their actions, and more closely links malfunctions in mTORC1-related genes to several diseases of aging.
"Our results begin to clarify how mTORC1-driven changes in crowding could cause the insides of human cells to solidify as a person ages, packing more proteins into the same space and interfering with functions that require them to move around," says senior study author Liam Holt, Ph.D., assistant professor in the Institute for Systems Genetics at NYU Langone Health. "This work may also help explain the origin of the solid protein clumps that appear in the cells of patients with cardiovascular diseases, diabetes and Alzheimer's."
Studies - Biologists - Cells - Survival - Limit
Based on past studies, biologists have long concluded that cells require for survival a limit on the number of proteins in their fluid-filled inner spaces, the cytoplasm where many cellular functions occur.
Specifically, the current study found that the mTORC1 complex controls crowding by determining the number of ribosomes, multi-protein machines that build other proteins there.
Engineering - Cells - Glowing - Tracers - Crowding
By engineering cells to make their own glowing tracers to measure crowding, the researchers showed that, by adjusting levels of mTORC1 action, they could cause a two-fold swing in the ability of multi-protein cellular...
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