Structural mechanism of TRPC3 channel activation by the moonwalker mutation
TRPC3 is a receptor-activated, non-selective cation channel expressed in the cerebellum and is critical for the proper development and function of Purkinje cells 1 . A gain-of-function mutation of TRPC3, T561A, leads to impaired dendritic arborization of Purkinje cells and cerebellar ataxia, manifesting as a distinctive moonwalker gait abnormality in mice 1 . Additionally, TRPC3 has increasingly been recognized for its involvement in immune responses, cancer progression, and various cardiovascular and neurological disorders, further underscoring its potential as a therapeutic target 2 .
Authors
- J. Zang (ORCID: https://orcid.org/0000-0003-2770-1387)
- Hailin Peng (ORCID: https://orcid.org/0000-0003-1569-0238)
- Lei Chen (ORCID: https://orcid.org/0000-0002-7619-8311)
- Wenjun Guo (ORCID: https://orcid.org/0009-0002-1789-7785)
- Yikun Chen (ORCID: https://orcid.org/0000-0001-9957-7851)
- Xiaole Zhao
- Yongmei Tan
Institutions
- Peking University (CN)
- Beijing National Laboratory for Molecular Sciences (CN)
- Center for Life Sciences (CN)
- State Key Laboratory of Membrane Biology (CN)
Publication Details
- Journal
- Cell Discovery
- Published
- 2026-10-29
- DOI
- https://doi.org/10.1038/s41421-026-00936-y
- Primary Topic
- Ion Channels and Receptors
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China