DGIST (Chairman Lee Geun-woo) announced that a research team led by Professor Byung Chan Seo of the Department of Neuroscience has elucidated for the first time a new molecular mechanism that controls the N-type voltage-gated calcium channel (CaV2.2), which plays an important role in nerve signal transmission. By uncovering the mechanism that controls the opening and closing of this channel, the research team has provided important clues for the development of future treatments for brain diseases.
Neurons transmit information to the next cell by converting electrical signals into chemical signals. A key step in this process is the influx of calcium ions into the cell through voltage-gated calcium channels. Professor Byung Chang Suh’s research team has uncovered the existence of so-called “molecular levers” that control this calcium channel and its regulatory mechanisms, providing an important foundation for the development of next-generation treatments for brain diseases.
The length of time that calcium channels remain open depends on the type of beta (β) subunit, an accessory protein that binds to the channel. However, the mechanism by which this subunit changes the structure of the channel was unknown until now.
Through comparative analysis of different beta subunit models, the research team discovered that a specific region of the channel where accessory proteins bind (R370, located at the beginning of the I-II loop) is unusually curved. The researchers also discovered that this loop pivots around R370 and acts like a “lever,” changing the structure of the channel to different degrees depending on the type of beta subunit it binds. The research team has now published the world’s first model showing how movements of this molecular lever change the structure of calcium channels.
Furthermore, by measuring the open and closed states of the channels using electrophysiological techniques and applying kinetic modeling, the research team demonstrated that these structural changes are important for neural signal transmission. This discovery is expected to be a new milestone in the development of therapeutic drugs for a wide range of intractable brain diseases involving calcium channels, including neuropathic pain, epilepsy, autism spectrum disorder, and Alzheimer’s disease.
Through this study, we clearly solved the long-standing question of how beta subunit binding causes dynamic conformational changes in calcium channels. We hope that the newly discovered molecular lever mechanism of calcium channels will greatly contribute to the development of new treatments for brain diseases in the future. ”
DGIST Department of Brain Science Professor Byung Chang Suh
This research was supported by the National Research Foundation of Korea’s Basic Research Institute, Leading Neuroscience Interdisciplinary Technology Development, and Core Individual Basic Research Program. The findings were published in the July 2026 issue of the magazine. Proceedings of the National Academy of SciencesJin-Nyung Woo, a student in the integrated bachelor’s, master’s, and doctoral program in DGIST’s Department of Neuroscience, is the lead author, and researcher Jeongeun Kim is a co-author.
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DGIST (Daegu Kyungbuk University of Science and Technology)
Reference magazines:
Wu, J.N.; others. (2026). The structural rigidity of the I-II loop couples Ca V β anchoring to the Ca V 2.2 gated mode. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2602744123. https://www.pnas.org/doi/10.1073/pnas.2602744123
