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Mon. Mar 17, 2025

Tue. Mar 18, 2025

Wed. Mar 19, 2025

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<strong>Targeting deubiquitination of Cav3.2 calcium as a new therapeutic strategy for treating pain </strong>

Ca2+ ions serve as a second messenger that is essential for life processes; however, excessive Ca2+ levels contribute to various diseases. In this symposium we will introduce (1) the mechanism of pain initiation via the Cav3.2-USP5 complex in DRG neurons and the development of therapeutic drugs targeting it (Zamponi), (2) TRPA1-mediated astrocytic Ca2+ signaling as an intrinsic protective response to vascular cognitive impairment (Shirakawa), (3) the role of RyR1 Ca2+-induced Ca2+ release (CICR) activity discovered from unique RyR1 mutant mice and its relationship to skeletal muscle diseases (Murayama), (4) the sex-specific mechanism of pulmonary arterial hypertension caused by calcium-sensing receptors discovered from comprehensive analysis (Yamamura), and (5) the mechanism by which Ca2+ channel molecular complexes contribute to vascular remodeling (Suzuki). This symposium is expected to share the achievements of the presenters in the field of Ca2+ signaling with an audience from a wide range of research fields, leading to the development of next-generation Ca2+ signaling research that is not limited to the organ being studied.

Ca2+ signaling-based diverse pathogenesis: Elucidation of molecular mechanisms and their application to drug discovery.

APPW2025

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[[OD]2S10m-4]Targeting deubiquitination of Cav3.2 calcium as a new therapeutic strategy for treating pain

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