SLC26A9

更新于：2025-05-07

基本信息

别名

Anion transporter/exchanger protein 9、anion transporter/exchanger-9、SLC26A9

+ [3]

简介

Ion transporter that can act both as an ion channel and anion exchanger (PubMed:15800055, PubMed:17673510, PubMed:26801567, PubMed:32818062). Mainly acts as a chloride channel, which mediate uncoupled chloride anion transport in an alternate-access mechanism where a saturable binding site is alternately exposed to either one or the other side of the membrane (PubMed:17673510, PubMed:26801567, PubMed:32818062). Also acts as a DIDS- and thiosulfate- sensitive anion exchanger the exchange of chloride for bicarbonate ions across the cell membrane (PubMed:11834742, PubMed:15800055).

关联

项与 SLC26A9 相关的药物

VS-009

靶点

CFTR x CaCC x SLC26A9

作用机制

CFTR调节剂 [+2]

在研机构

Nuvara Therapeutics

原研机构

Nuvara Therapeutics

在研适应症

肺囊性纤维化

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SLC26A9 相关的临床结果

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100 项与 SLC26A9 相关的转化医学

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0 项与 SLC26A9 相关的专利（医药）

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120

项与 SLC26A9 相关的文献（医药）

2025-03-01·Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

SLC26A9 promotes the initiation and progression of breast cancer by activating the PI3K/AKT signaling pathway

Article

作者: An, Jiaxing ; Liu, Xuemei ; Lu, Chengli ; Jin, Hai ; Wen, Guorong ; Wang, Hu ; Ma, Zhiyuan ; Zhang, Minglin ; Li, Taolang ; Tuo, Biguang ; Yi, Zhiqiang ; Zhao, Yingying ; Zhou, Zhengxing ; Yuan, Peng ; Zhang, Chengmin ; Deng, Zilin ; Mu, Renmin ; Zhu, Jiaxing

SLC26A9 is a member of the Slc26a family of multifunctional anion transporters that function as Cl^- channels in the stomach. We reported for the first time that SLC26A9 is involved in gastric tumorigenesis. However, the role of SLC26A9 in breast cancer has not yet been investigated. We first demonstrated that the upregulation of SLC26A9 is associated with the clinicopathological progression and poor prognosis of patients with breast cancer and is positively correlated with HER2 amplification. SLC26A9 alters the proliferation, migration, and invasion potential of breast cancer cells by regulating the PI3K/AKT signaling pathway. SLC26A9 acts as an oncogene in the development of breast cancer. These findings provide valuable insights for the development of future diagnostic and therapeutic strategies for BC.

2025-03-01·Poultry Science

Probiotics improve eggshell quality via regulating microbial composition in the uterine and cecum

Article

作者: Hu, Zhi ; Lu, Yuxiang ; Rustempasic, Alma ; Zhou, Yuxin ; Zhang, Yao ; Liu, Yiping ; Zhao, Xiaoling ; Xu, Hengyong ; Wang, Yan ; Pu, Jiaxue ; Deng, Qingqing ; Li, Dan

Probiotics benefit the health and production performance of chickens, but their impact on egg and eggshell quality, particularly in the later stage, remains unclear. Here, 1-day-old Tianfu green shell-laying hens were fed either non-probiotics feed (n = 180) or feed supplemented with 100 mg / kg probiotics (n = 180). 16S rDNA sequencing indicated that dietary probiotics decreased the distribution of uterine p_Firmicutes, g_Fusobacterium, and s_Fusobacterium_unclassified, while increased p_Proteobacteria, g_Ralstonia, and s_Ralstonia_unclassified. PICRUSt2 and Bug Base analysis revealed enrichment in fatty acid metabolism, thiamine metabolism, vitamin B6 metabolism pathways and increased relative abundance of Proteobacteria, Firmicutes, Bacteroidetes. With LDA > 4.5, 35 and 25 marker bacterial taxa were identified in the uterus and cecum, respectively. Probiotics significantly increased uterine villi length and width, and the expressions of ATP2B2,SLC26A9,TF,OC-17,OCX-32, and OVAL in the uterus at the early and peak laying stage. Meantime, probiotics improved egg quality, pore density of eggshell barrier layer, and levels of Ca²⁺, Na⁺, and Mg²⁺, whereas dropped levels of P^3-, S^2- and K⁺ in eggshell. In serum, Ca²⁺, K⁺, Na⁺ had a response to dietary probiotics at different laying stages, except Cl^-. Furthermore, the changes of these phenotypes are closely related to the microbial structure of the uterus and cecum. Overall, the data suggest that dietary probiotics improved uterine and cecal microbiota, optimized egg quality, eggshell quality, uterus development, and regulated mineralization gene expression and ion content in serum and eggshell, thereby improving productivity of laying hens. These results provide reference for the application of probiotics in the laying industry.

2025-02-01·Journal of Biological Chemistry

Disorder within order: Identification of the disordered loop of STAS domain as the inhibitory domain in SLC26A9 chloride channel

Article

作者: Romero, Michael F ; Chen, An-Ping ; Chang, Min-Hwang ; Decker, James W ; Holmes, Heather

The chloride transporter-channel SLC26A9 is mediated by a reciprocal regulatory mechanism through the interaction between its cytoplasmic sulfate transporter and anti-sigma (STAS) domain and the R domain of cystic fibrosis (CF) transmembrane regulator. In vertebrate Slc26a9s, the STAS domain structures are interrupted by a disordered loop which is conserved in mammals but is variable in nonmammals. Despite the numerous studies involving the STAS domains in SLC26 proteins, the role of the disordered loop region has not been identified. Deletion of the entire Slc26a9-STAS domain results in loss of Cl^- channel function. Surprisingly, we found that partial or full deletion of the STAS-disordered loop substantially increases the SLC26A9 chloride transport-channel activity. Bioinformatics analysis reveals that the disordered loops there are three subregions: a K/R-rich region, a "middle" region, and an ordered S/T-rich motif. In this study, the role of this STAS-disordered loop is investigated by using serial deletions and the ordered S/T-rich motif is examined by serial alanine substitution. Substitutions of alanine for serine or threonine in the 620 to 628 S/T-rich motif decrease SLC26A9 chloride channel activity. These experiments parse the functional roles of SLC26A9-STAS-disordered loop and its subdivisions modifying overall SLC26A9 activities. Recently, SLC26A9 has emerged as one of the potential substitutes for abnormal CF transmembrane regulator in CF. Our findings suggest that deletion of variable loop of human SLC26A9 may provide a new gene therapy strategy in the treatment of CF disease.