ANO6

更新于：2025-05-07

基本信息

别名

ANO6、anoctamin 6、Anoctamin-6

+ [5]

简介

Small-conductance calcium-activated nonselective cation (SCAN) channel which acts as a regulator of phospholipid scrambling in platelets and osteoblasts. Phospholipid scrambling results in surface exposure of phosphatidylserine which in platelets is essential to trigger the clotting system whereas in osteoblasts is essential for the deposition of hydroxyapatite during bone mineralization. Has calcium-dependent phospholipid scramblase activity; scrambles phosphatidylserine, phosphatidylcholine and galactosylceramide (By similarity). Can generate outwardly rectifying chloride channel currents in airway epithelial cells and Jurkat T lymphocytes. (Microbial infection) Upon SARS coronavirus-2/SARS-CoV-2 infection, is activated by spike protein which increases the amplitude of spontaneous Ca(2+) signals and is required for spike-mediated syncytia.

关联

100 项与 ANO6 相关的临床结果

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100 项与 ANO6 相关的转化医学

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0 项与 ANO6 相关的专利（医药）

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261

项与 ANO6 相关的文献（医药）

2025-05-01·Cell Reports

Anoctamins mediate polymodal sensory perception and larval metamorphosis in a non-vertebrate chordate

Article

作者: Chatzigeorgiou, Marios ; Liang, Zonglai ; Hoyer, Jorgen

The ocean represents a complex sensory environment, which acts as a crucible of evolution for polymodal sensory perception. The cellular and molecular bases of polymodal sensory perception in a marine environment remain enigmatic. Here, we use Ca²⁺ imaging and quantitative behavioral analysis to show that in the tunicate Ciona intestinalis, two members of the evolutionarily conserved anoctamin family (Tmem16E/Ano5 and Tmem16F/Ano6) are required for sensing chemosensory and mechanosensory metamorphic cues. We find that they modulate neuronal excitability and Ca²⁺ response kinetics in the primary sensory neurons and axial columnar cells of the papillae. Chemogenetic perturbations suggest that Ano5 and Ano6 act downstream of the primary sensory transducer molecules. Using pharmacology, we show that Ano5 and Ano6 cooperate with the inositol 1,4,5-trisphosphate (IP₃) receptor and calcium release-activated channels (CRACs) to modulate tail regression. Our results establish Ano5 and Ano6 as players in the zooplanktonic molecular toolkit that controls polymodal sensory perception in aquatic environments.

2025-04-01·Life Sciences

Benzbromarone improves blood hypercoagulability after TBI by reducing phosphatidylserine externalization through inhibition of TMEM16F expression

Article

作者: Gao, Yalong ; Peng, Ruilong ; Li, Lei ; Li, Kaiji ; Zhang, Jianning ; Chen, Xin ; Li, Tuo ; Zhang, Shu ; Wang, Jinchao ; Wang, Cong ; Yang, Guili

AIMSTraumatic brain injury-induced coagulopathy (TBI-IC) frequently occurs after TBI, exacerbating the severity of TBI and affecting patient prognosis. Benzbromarone (BBR) is commonly used to treat hyperuricemia; however, its protective effects against TBI-IC remain unknown. Therefore, we explored whether BBR could improve TBI.MATERIALS AND METHODSC57BL/6 wild-type mice were subjected to fluid percussion injury to mimic TBI, and BBR was administered intraperitoneally 30 min after TBI. Magnetic resonance imaging (MRI) and Evans blue dye extravasation were used to assess the prognosis, tail bleeding time, ELISA, and coagulation tests assess coagulation function. We further explored the potential mechanism by which BBR alleviates hypercoagulation after TBI using flow cytometry.KEY FINDINGSThe intraperitoneally injected BBR group showed improved survival and neurological severity scores compared to the TBI group. Subsequently, we found that hypercoagulability developed 3 h after TBI and that the administration of BBR improved this hypercoagulability. BBR also reduced the degree of platelet phosphatidylserine (PS) exposure after TBI, platelet activation, and Ca2+ overload, in addition to inhibition of scramblase activity in procoagulant platelets.SIGNIFICANCEOur findings indicate that BBR reduces PS externalization by inhibiting TMEM16F expression, thereby improving blood hypercoagulability after TBI.

2025-04-01·Gene

Identification of novel hub gene and biological pathways associated with ferroptosis in In-Stent restenosis

Article

作者: Zhang, Meixia ; Guo, Yunmiao ; Huang, Siming ; Xu, Huiling ; Pang, Lijuan ; Du, Jin ; Zhao, Xia ; Cai, Wenping ; Qiu, Jin ; Tao, Lin ; Jin, Shan ; Xu, Lingli

BACKGROUNDIn-stent restenosis (ISR) is one of the most significant complications following percutaneous coronary intervention (PCI) in patients with coronary artery disease (CAD). Ferroptosis is a novel cell death mode characterized by iron overload and lipid peroxidation. However, the role of ferroptosis in vascular smooth muscle cells (VSMCs) regulating neointimal formation during restenosis remains unclear.OBJECTIVEThe current study aims to reveal the molecular targets for neointimal hyperplasia through integrated analysis of data from gene expression omnibus (GEO) databases and single-cell sequencing (scRNA-Seq).METHODS AND RESULTSIn this study, we screened ten common differentially expressed genes (Co-DEGs) including BID, SP1, NCF2, HERPUD1, RICTOR, LAMP2, CAT, ACSL1, CS, and ANO6 from the GEO and FerrDb V2. GO/KEGG analyses indicated that metabolic reactions, particularly glyoxylate and dicarboxylate metabolism pathways, are the main molecular events. Immune infiltration analysis showed significant correlations between the expression of Co-DEGs and the infiltration of macrophages, dendritic cells, eosinophils, and neutrophils. Moreover, we identified SP1 as a potential therapeutic target associated with ferroptosis in ISR and constructed a lncRNA-miRNA-SP1 regulatory network. Using scRNA-Seq data to validate the expression of Co-DEGs in the neointima, we found that metabolic pathways such as carbon metabolism, peroxisomes, and reactive oxygen species were enriched. Immune infiltration examined the relationship between Co-DEGs and immune cells, revealing negative correlation between SP1 and neutrophils, and positive correlation between BID and macrophages.CONCLUSIONThe integrated analyses identified SP1 as a key regulator of ferroptosis in ISR and proposed its potential to be a novel therapeutic target of ISR. The construction of ceRNA network based on SP1 might contribute to new treatment strategy and drug development for ISR.

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