Filamin interacts with epithelial sodium channel and inhibits its channel function.

Epithelial sodium channel (ENaC) in the kidneys is critical for Na(+) balance, extracellular volume, and blood pressure. Altered ENaC function is associated with respiratory disorders, pseudohypoaldosteronism type 1, and Liddle syndrome. ENaC is known to interact with components of the cytoskeleton, but the functional roles remain largely unclear.

Receptor for activated C kinase 1 (RACK1) inhibits function of transient receptor potential (TRP)-type channel Pkd2L1 through physical interaction.

Pkd2L1 (also called TRPP3) is a non-selective cation channel permeable to Ca(2+), Na(+), and K(+) and is activated by Ca(2+). It is also part of an acid-triggered off-response cation channel complex. We previously reported roles of the Pkd2L1 C-terminal fragments in its channel function, but the role of the N terminus remains unclear.