|Professor Kim Hyun-jin (news.joins.com)|
A research team led by Kim Hyun-jin, a professor of the Department of Physiology at the School of Medicine, has discovered a new process to regulate autophagy, which is an intracellular degradation system where subcellular organelles are destroyed and new ones are built to replace them to help a body cleanse itself. In previous studies, the fact that intracellular calcium (Ca2+) signaling regulated autophagy was already discovered; how the Ca2+ channel was related to autophagy was not known. The research team succeeded in discovering that activating MCOLN3/TRPML3, a Ca2+ permeable ion channel, could regulate autophagy and that palmitoylation was required for dynamic trafficking and cellular function of MCOLN3/TRPML3 in autophagy. Palmitoylation, which is the covalent attachment of deprotonated fatty acids, regulated not only MCOLN3/TRPML3 trafficking to autophagic structures but also autophagic flux. The researchers reported that the activation of intracellular MCOLN3/TRPML3 induced Ca2+ release, which increased autophagy depending on Ca2+ and palmitoylation. When nutritionally deficient, MCOLN3/TRPML3 was activated to release Ca2+ and increased the level of MCOLN3/TRPML3 palmitoylation. Without MCOLN3/TRPML3 palmitoylation, however, the induced MCOLN3/TRPML3 was disrupted. It is the first time to discover MCOLN3/TRPML3 as a new autophagy regulator, and the research is expected to contribute to the discovery of treatments for autophagic diseases such as cancer or degenerative diseases. The research result was published on the website of the international journal Autophagy, which published the research papers of the autophagic studies, on September 6th.
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