Fig. 6.

Hypothetical role of TRPP2 in mechanotransduction. Cilium bending in response to fluid shear stress may activate GPCR(s) in a ligand-independent fashion, probably through mechanical stretching of the PM and/or associated cytoskeletal structures (arrows). Activation of GPCR would result in intracellular Ca²⁺ release from the ER through the IP₃ pathway and activation of SOCs. ROCs, including plasma membrane TRPP2, could also be activated, resulting in a massive and long-lasting increase in intracellular Ca²⁺ concentration. Dashed arrow denotes changes in membrane tension in response to cilium bending.