A potential gain-of-function variant of SLC9A6 leads to endosomal alkalinization and neuronal atrophy associated with Christianson Syndrome-论文-万方医学网

A potential gain-of-function variant of SLC9A6 leads to endosomal alkalinization and neuronal atrophy associated with Christianson Syndrome

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作者： Ilie, Alina ^[1] ; Gao, Andy Y. L. ^[2] ; Boucher, Annie ^[3] ; Park, Jaeok ^[4] ; Berghuis, Albert M. ; Hoffer, Mariette J. V. ; Hilhorst-Hofstee, Yvonne ; McKinney, R. Anne ; Orlowski, John

作者单位： Dept Physiol,McGill Univ ^[1] Dept Pharmacol & Therapeut,McGill Univ ^[2] Dept Biochem,McGill Univ ^[3] Dept Clin Genet,Leiden Univ ^[4]

关键词 Christianson Syndrome X-linked intellectual disability Alkali cation/proton exchangers-SLC9A6/NHE6 Endosomal pH homeostasis Membrane trafficking Neurodegeneration NA+/H+ EXCHANGER NHE6 DENDRITIC SPINES EXTRACELLULAR VESICLES PHENOTYPIC SPECTRUM MENTAL-RETARDATION ESCHERICHIA-COLI MEMBRANE PH TRANSFERRIN CHLOROQUINE

发布时间 2022-12-22

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A potential gain-of-function variant of SLC9A6 leads to endosomal alkalinization and neuronal atrophy associated with Christianson Syndrome

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A potential gain-of-function variant of SLC9A6 leads to endosomal alkalinization and neuronal atrophy associated with Christianson Syndrome

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