We are grateful to all the authors and collaborators who made this study possible. Special thanks to everyone in the Cordero-Morales and Vásquez laboratories (especially Briar Bell, Angela Jaramillo-Granda, and Luis Romero), as well as to our collaborators.
www.science.org/doi/10.1126/... (3/4)
Structural snapshots capture an ataxia-linked overactive ion channel in its open state and reveal a druggable site for inhibition.
We are so happy to see Vasanthi Jayaraman named chair of Biochemistry at UTHouston
Vasanthi is not only a leader in biophysics and Editor-in-Chief of the Biophysical Journal, but also a wonderful colleague and mentor
Congratulations @frettinglab.bsky.social
med.uth.edu/blog/2026/04...
Sudha (@chakrapanilab.bsky.social) and Julio (@cvlab.bsky.social) are organizing the 2026 Ion Channel Gordon Research Conference: Ion Channels Across Scales — Bridging Molecular Events to Physiological Outcomes, to be held at Mount Holyoke College, July 12–17, 2026.
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McGovern Medical School is the eleventh largest medical school in the United States. Located in the heart of the Texas Medical Center, the school was established by the Texas Legislature in 1969 to ad...
med.uth.edu
Here is the morph video summarizing some of the changes we found in a TRPC3 hypermorphic variant (Science Advances, Science Magazine)
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A great opportunity to bring trainees, exchange ideas, and connect across disciplines. Registration is open: www.grc.org/ion-channels...
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We have an outstanding speaker lineup, including Keynote Talks by Kenton Swartz, Nancy Carrasco, Miriam B. Goodman (@wormsense.bsky.social), and Francisco Bezanilla. Trailblazer Spotlights presented by Ed Twomey (@cryoet.bsky.social)and Theanne Griffith (@doctheagrif.bsky.social).
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Using electrophysiology, cryo-EM, molecular simulations, and in vivo models, we also identify a druggable inhibitory site that could guide future therapies for cerebellar ataxia.
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Video
Excited to share our new paper in Science Advances @science.org
In this work, we uncover how a disease-linked TRPC3 mutation, together with a cerebellum-specific splice isoform, stabilizes the channel in an open state, drives Calcium overload, and promotes neurodegeneration. (1/4)
