LRRC8A channels support TNFα-induced superoxide production by Nox1 which is required for receptor endocytosis

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• 作者：Hyehun Choi^a ; Nicholas Ettinger^b ; Jeffrey Rohrbough^a ; Anna Dikalova^a ; Hong N. Nguyen^a ; Fred S. Lamb^a ; ^{fred.s.lamb@vanderbilt.edu}
• 关键词：Ad ; adenovirus ; BCA ; bicinchoninic acid ; BSA ; bovine serum albumin ; CAT1H ; 1-Hydroxy-2 ; 2 ; 6 ; 6-tetramethylpiperidin-4-yl-trimethylammonium chloride ; DMEM ; Dulbecco's modified Eagle's medium ; DynK44A ; dominant-negative dynamin ; eGFP ; enhanced green fluorescent protein ; ERK ; extracellular signal-regulated kinase ; ESR ; electron spin resonance ; FBS ; fetal bovine serum ; FITC ; Fluorescein isothiocyanate ; iNOS ; inducible nitric oxide synthase ; JNK ; c-Jun N-terminal kinase ; LRRC8 ; Leucine Rich Repeat Cont
• 刊名：Free Radical Biology and Medicine
• 出版年：2016
• 出版时间：December 2016
• 年：2016
• 卷：101
• 期：Complete
• 页码：413-423
• 全文大小：2093 K
• 卷排序：101

文摘

Nox1 activation by TNFα requires functional LRRC8A anion channels. TNFα receptor endocytosis requires Nox1-derived extracellular O2 -. JNK provides negative feedback regulation of Nox1 at the plasma membrane. Nox1-LRRC8A interdependence may allow anion channel blockers to inhibit inflammation.