This recombinant Human KCNK3 protein is a full-length protein expressed in vitro using an E.coli cell-free expression system. Its purity is greater than 85%, as determined by SDS-PAGE. Cell-free protein expression refers to the in vitro synthesis of a protein utilizing translation-compatible extracts from whole cells. These extracts contain all the necessary macromolecules and components for transcription, translation, and even post-translational modifications. These components include RNA polymerase, regulatory protein factors, transcription factors, ribosomes, and tRNA. When supplemented with cofactors, nucleotides, and the specific gene template, these extracts can synthesize proteins of interest within a few hours.
KCNK3 is an acid-sensitive potassium channel responsible for regulating the resting membrane potential of human pulmonary artery smooth muscle cells (PASMCs). It mediates outward potassium ion currents to counteract depolarization-induced calcium ion influx. Mutations in KCNK3 have been linked to rare cases of both familial and idiopathic pulmonary arterial hypertension (PAH). The reduced KCNK3 activity resulting from these mutations likely leads to depolarization of the resting membrane potential, potentially causing vasoconstriction and pulmonary artery remodeling. Additionally, KCNK3 negatively modulates thermogenesis by inhibiting cAMP-PKA signaling.