Dysregulated Ca<sup>2+</sup> signaling, fluid secretion, and mitochondrial function in a mouse model of early Sjögren's syndrome.

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第一作者： Kai-Ting,Huang

第一单位： Department of Pharmacology and Physiology, University of Rochester, 601 Elmwood Avenue, Rochester, NY. 14526.

作者： Kai-Ting,Huang ^[1] ; Larry E,Wagner ^[1] ; Takahiro,Takano ^[1] ; Xiao-Xuan,Lin ^[1] ; Harini,Bagavant ^[2] ; Umesh,Deshmukh ^[2] ; David I,Yule ^[1]

作者单位： Department of Pharmacology and Physiology, University of Rochester, 601 Elmwood Avenue, Rochester, NY. 14526. ^[1] Arthritis and Clinical Immunology, Oklahoma Medical Research Foundation, 825 NE 13 Street, Oklahoma City, OK 73104. ^[2]

关键词 Ca2+ signaling DMXAA-induced SS mouse model Salivary gland hypo-function Sj?gren’s syndrome TMEM16a channel Xerostomia mitochondrial dysfunction

DOI 10.1101/2024.03.19.585719

PMID 38562738

发布时间 2024-10-23

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Dysregulated Ca<sup>2+</sup> signaling, fluid secretion, and mitochondrial function in a mouse model of early Sjögren's syndrome.

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Dysregulated Ca<sup>2+</sup> signaling, fluid secretion, and mitochondrial function in a mouse model of early Sjögren's syndrome.

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