Phosphorylation of distal C-terminal residues promotes TRPV4 channel activation in response to arachidonic acid.

Transient receptor potential vanilloid 4 (TRPV4) is a Ca-permeable channel activated by diverse physical and chemical stimuli, including mechanical stress and endogenous lipid arachidonic acid (AA) and its metabolites. Phosphorylation of TRPV4 by protein kinase A (PKA) and protein kinase C (PKC) is a predominant mechanism for channel regulation, especially in the cytoplasmic domains due to their importance in protein assembly, and channelopathies. However, studies corresponding to phosphorylation sites for these kinases remain incomplete.