Silencing of Kir2 channels by caveolin-1: cross-talk with cholesterol.

摘要: A growing number of studies show that different types ion channels localize in caveolae and are regulated by the level membrane cholesterol. Furthermore, it has been proposed cholesterol-induced regulation might be attributed to partitioning into association with caveolin-1 (Cav-1). We tested, therefore, whether Cav-1 regulates function inwardly rectifying potassium Kir2.1 play major roles potentials numerous mammalian cells. Our earlier demonstrated cholesterol sensitive. In this study, we co-immunoprecipitate co-expression HEK293 cells results suppression Kir2 current indicating is a negative regulator function. These observations confirmed comparing Kir currents bone marrow-derived macrophages isolated from Cav-1(-/-) wild-type animals. also show, however, maintain their sensitivity have very low levels endogenous knockout mice. Thus, these indicate and/or intact not required for channels. Moreover, single point mutation Kir2.1, L222I abrogates abolishes suggesting two modulators regulate via common mechanism.