ArfGAP2 promotes STING proton channel activity, cytokine transit, and autoinflammationArfGAP2 is a dual regulator of STING signaling and proton efflux in specific cell types, with STING proton channel activity regulating Golgi transit and secretion of cytokines. Autoinflammatory disease caused by hyperactivity of STING in mice can be ameliorated through reduction of ArfGAP2.ArfGAP2 is a dual regulator of STING signaling and proton efflux in specific cell types, with STING proton channel activity regulating Golgi transit and secretion of cytokines. Autoinflammatory disease caused by hyperactivity of STING in mice can be ameliorated through reduction of ArfGAP2.Subhajit Poddar, Samuel D. Chauvin, Christopher H. Archer, Wei Qian, Jean A. Castillo-Badillo, Xin Yin, W. Miguel Disbennett, Cathrine A. Miner, Joe A. Holley, Teresa V. Naismith, W. Alexander Stinson, Xiaochao Wei, Yue Ning, Jiayuan Fu, Trini A. Ochoa, Nehalee Surve, Shivam A. Zaver, Kimberly A. Wodzanowski, Katherine R. Balka, Rajan Venkatraman, Canyu Liu, Kelly Rome, Will Bailis, Yoko Shiba, Sara Cherry, Sunny Shin, Clay F. Semenkovich, Dominic De Nardo, Sunnie Yoh, Elisha D.O. Roberson, Sumit K. Chanda, David J. Kast, Jonathan J. Minerhttps://www.cell.com/cell/fulltext/S0092-8674(25)00096-0?rss=yeshttp://www.cell.com/cell/inpress.rssCellCell RSS feed.Wireless News CampaignFebruary 13, 2025

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