The organic anion transporter SLCO2A1 constitutes the core component of the Maxi‐Cl channel

• Published in: The EMBO journal Vol. 36; no. 22; pp. 3309 - 3324
• Main Authors: Sabirov, Ravshan Z, Merzlyak, Petr G, Okada, Toshiaki, Islam, Md Rafiqul, Uramoto, Hiromi, Mori, Tomoko, Makino, Yumiko, Matsuura, Hiroshi, Xie, Yu, Okada, Yasunobu
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 15.11.2017; John Wiley and Sons Inc
• Subjects: Adenosine Triphosphate - metabolism; Amphibians; Animals; anion channel; Anion channels; Anions; ATP; Cell Fractionation; Cell lines; Cell Membrane - drug effects; Cell Membrane - metabolism; Conductance; CRISPR; CRISPR-Cas Systems - genetics; Dinoprostone - pharmacology; Female; Fluxes; Gene Deletion; Gene Silencing - drug effects; Genetic screening; Green Fluorescent Proteins - metabolism; HEK293 Cells; Humans; Ion Channel Gating - drug effects; Ion channels; Ion Channels - metabolism; Ischemia; Maxi‐Cl; Membrane Proteins - metabolism; Mice, Inbred C57BL; molecular entity; Mutation - genetics; organic anion transporter; Organic Anion Transporters - metabolism; Protein transport; Proteins; Proteolipids - drug effects; Proteolipids - metabolism; Proteomics; Recombinant Proteins - metabolism; Reperfusion; Reperfusion Injury - pathology; Resistance; RNA-mediated interference; Rodents; Screening; siRNA; SLCO2A1; organic anion transporter; Maxi‐Cl; molecular entity; anion channel; SLCO2A1

The maxi‐anion channels (MACs) are expressed in cells from mammals to amphibians with ~60% exhibiting a phenotype called Maxi‐Cl. Maxi‐Cl serves as the most efficient pathway for regulated fluxes of inorganic and organic anions including ATP. However, its molecular entity has long been elusive. By s...