[Asia Economy Reporter Hwang Junho] Domestic researchers have developed a new method to analyze proteins within cells and discovered proteins that regulate communication between cellular organelles. Among them, they identified a protein that can regulate the increase of calcium in mitochondria within cells. This protein is expected to become a new target for developing treatments for Alzheimer's disease and Parkinson's disease in the future.
The Korea Brain Research Institute announced on the 2nd that a joint research team involving Seoul National University and POSTECH discovered a protein involved in the formation of intracellular signaling hubs. Mitochondria, the organelles that supply energy within our body's cells, and the endoplasmic reticulum, which produces and transports proteins, are connected through a membrane called MAM that acts as a signaling hub. The proteins that make up this membrane regulate key functions such as intracellular lipid metabolism and autophagy.
The research team devised a new technique called Contact-ID to label and analyze proteins located in MAM, identifying 115 proteins that constitute MAM in living human cells. Additionally, using large-area three-dimensional electron microscopy to observe the MAM region inside cells in 3D, the team revealed that the FKBP8 protein changes the connection structure (MAM) between mitochondria and the endoplasmic reticulum and plays an essential role in calcium transport.
The research team found significance in discovering a protein that can regulate the increase of calcium in mitochondria, which is known as a common cause of neurodegenerative diseases. They expect this protein to be used as a new target for developing treatments for Alzheimer's disease, Parkinson's disease, and other conditions in the future.
Dr. Moon Ji-young stated, "When the network between cellular organelles is not properly formed, diseases occur. We have more accurately identified the MAM proteins involved in this process," adding, "Among these proteins, we conducted collaborative research on the function of FKBP8 and plan to carry out follow-up studies on its role as a key factor that can delay or prevent mitochondrial damage." The results of this study were published in the May issue of the scientific journal Proceedings of the National Academy of Sciences (PNAS).
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