Ask about this productRelated genes to: SLC26A9 antibody
- Gene:
- SLC26A9 NIH gene
- Name:
- solute carrier family 26 member 9
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-25
- Date modifiied:
- 2016-02-17
Related products to: SLC26A9 antibody
Related articles to: SLC26A9 antibody
- Cystic fibrosis-related diabetes (CFRD) is a common metabolic complication in adolescents with cystic fibrosis (CF). Variants in and have been implicated in CFRD susceptibility. The coexistence of CF, CFRD, and celiac disease in childhood is rare and presents diagnostic and therapeutic challenges. We describe a 14-year-old female with CF carrying compound heterozygous mutations (p.Glu831Ter and ). Sweat chloride values were borderline. At age 7, she was diagnosed with celiac disease after elevated anti-tTG IgA (297 U/mL) and IgG (22.6 U/mL) and was started on a gluten-free diet. At age 12 years, she presented with diabetic ketoacidosis and was diagnosed with CFRD, requiring insulin therapy. Genotyping revealed high-risk diabetes and CF-modifier variants: rs7903146 TT () and rs4077468 GG (). This case highlights the interplay of CF, autoimmunity, and genetic predisposition in early onset CFRD. Genetic profiling may improve risk assessment in CF patients with complex endocrine or autoimmune presentations. - Source: PubMed
Publication date: 2026/03/16
Kvaratskhelia EkaAgladze DodoVardosanidze NinoGhughunishvili MariamSurmava SandroAbzianidze EleneTkemaladze Tinatin - While cystic fibrosis is caused by loss-of-function variants in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), other modifier genes have been shown to associate with disease severity. Co-expression of modifiers with CFTR in normal tissue indicates a cooperative relationship and suggests the potential for compensation in the presence of CFTR dysfunction. We examined the co-expression relationships with CFTR in the lung using single cell RNA sequencing to pinpoint cell types and their modifiers involved in the cystic fibrosis lung phenotype and support target prioritization for therapy. SmartSeq2 single cell RNA sequencing data on non-cystic fibrosis lung tissue was used for evaluation of co-expression with CFTR and modifier genes. A zero-inflated negative binomial model was used to formally test the co-expression association. 10X Chromium based single cell RNA sequencing data from both cystic fibrosis and non-cystic fibrosis studies were assessed graphically to confirm conclusions from the SmartSeq2 primary analysis. Differentiating basal, club and alveolar epithelial type 2 cells were found to have high proportions of cells expressing CFTR as well as the greatest number of significant co-expression relationships with the modifiers. In particular, among alveolar epithelial type 2 cells, we observed a significant co-expression trio relationship between CFTR, SLC6A14 and SLC26A9 (p < 0.05). CFTR-modifier gene co-expression suggests basal, club and alveolar epithelial type 2 cells show coordinated expression. Alveolar epithelial type 2 cells showed strong co-expression evidence with two of the most established cystic fibrosis modifier genes. - Source: PubMed
Publication date: 2025/12/02
Wang ChengKanagarajah KayshaniWong AmyRatjen FelixStrug Lisa J - Triple-negative breast cancer (TNBC) presents significant clinical challenges due to its high heterogeneity and lack of effective targeted therapies. Cancer stem cells (CSCs) play a crucial role in TNBC recurrence, metastasis, and drug resistance. However, the interplay between ion transport, microenvironmental regulation, and classical stemness pathways remains underexplored in existing reviews. In this work, we systematically integrated multi-omics databases, network pharmacology, protein-protein interaction (PPI) analysis, functional pathway enrichment, and molecular modeling to highlight the "bridging" role of SLC26A9 and its interacting proteins in TNBC stem cell self-renewal, drug resistance, and microenvironmental regulation. Comprehensive molecular docking and 100-ns molecular dynamics (MD) simulations demonstrated that the small molecule S9-A13 exhibited high affinity and stable binding to both SLC26A9 and tumor protein p53 (TP53), with docking affinities of -7.737 and -8.447 kcal/mol and molecular mechanics/generalized Born surface area (MM/GBSA) binding free energies of -34.47 and -25.65 kcal/mol, respectively. These results suggest that S9-A13 may act on the SLC26A9-TP53 axis to enable multi-target regulation of TNBC cancer stem cells. We further discuss the translational implications of such interventions, including safety profile considerations, potential off-target effects, and delivery strategies. In summary, this review provides a structured framework and testable hypotheses for developing SLC26A9-based multi-target precision therapies for TNBC CSCs, while emphasizing that these computational findings are hypothesis-generating and require rigorous experimental and clinical validation prior to translation. - Source: PubMed
Publication date: 2025/11/13
Shen MimiMa ZhiyuanCao YanghuiWang LanFeng GuoliZhou ZhengxingLi LeileiJi BeiLiu ShuhuiQin JiaqiWang QinLiu XuemeiLi Taolang - Perineural invasion (PNI) is a pivotal prognostic factor in pancreatic ductal adenocarcinoma (PDAC), associated with aggressive tumor behavior and poor patient outcomes. This study investigated the role of Slc26a9 in regulating peripheral nerve invasion in pancreatic cancer. Bioinformatic analysis of GEO datasets showed markedly higher Slc26a9 expression in PNI-positive patients than in those without PNI. A PDAC model was established by implanting Panc02-luc cells into C57BL/6 mice. Abdominal mechanical hyperalgesia, hunching behavior, and anxiety-like behaviors were assessed using von Frey, hunch-score, and open field tests. PNI in pancreatic tissue was evaluated by immunohistochemistry. On postoperative days 7, 14, and 21, PDAC mice exhibited significantly increased tumor volume and weight, and decreased spleen weight (days 14 and 21) compared to the sham group. By day 21, body weight was also significantly reduced. On day 7, there were no significant differences in mechanical sensitivity, hunch scores, or anxiety-like behaviors, and no PNI was observed. By day 14, PDAC mice showed marked increases in pain, hunch scores, and anxiety-like behaviors, accompanied by evidence of PNI. To further explore the mechanism, we engineered a Slc26a9-overexpressing Panc02 cell line. Transwell and scratch assays demonstrated that Slc26a9 overexpression promotes Panc02 cell migration in vitro. In vivo, mice implanted with Slc26a9-overexpressing cells exhibited pronounced abdominal mechanical hyperalgesia, elevated hunch scores, and anxiety-like behaviors as early as day 7, along with confirmed PNI in the pancreas. These results suggest that Slc26a9 facilitates PNI in pancreatic cancer and may serve as a promising therapeutic target. - Source: PubMed
Publication date: 2025/11/08
Hua BohanHuang XiaogengChen LipingLi YuhuaLu DashanWang DongjieChen YujingNi HuadongYao MingNi Chaobo - Cystic fibrosis (CF) is characterized by impaired chloride and bicarbonate secretion due to mutations in the CFTR gene which codes for a plasma membrane anion channel. Defective anion transport in CF is particularly severe in the respiratory system, with impairment of mucociliary clearance, mucus accumulation, and airway obstruction. Pharmacological CFTR modulators, able to rescue mutant CFTR trafficking and gating, have improved the clinical condition of many CF patients, particularly those with F508del mutation. However, there is a substantial number of patients with mutations unresponsive to CFTR modulators. This unmet need has prompted the exploration of alternative therapies to target the basic defect in CF. This review provides a comprehensive overview covering the years 2010-2025 of most prominent advances in the identification of small-molecule inhibitors and activators targeting three potential contributors to airway epithelium ion homeostasis: pendrin (SLC26A4), SLC26A9, and TMEM16A (ANO1). These molecules may represent potential therapeutic agents and/or be important tools of research to understand the pathophysiological role of their target. For pendrin, high-throughput screening yielded novel classes of potent and selective inhibitors including tetrahydropyrazolopyridines and pyrazolo-thiophenesulfonamides. SAR analysis led to the discovery of lead compounds PDSinh-A01 and PDSinh-C01 showing significant activity and favourable drug-like properties. Additionally, 5-benzyloxy-2-methylbenzofuran compounds have emerged as promising candidates with increased activity and favourable drug-like properties. Though SLC26A9 involvement in chloride secretion remains debated, the identification of the potent and selective inhibitor S9-A13 revealed the role of this transporter in ASL pH regulation via bicarbonate modulation. Pharmacological potentiation of TMEM16A, a calcium activated chloride channel, could be a way to bypass the defective anion transport in CF. To achieve this goal, the ETX001 compound was identified and progressed to clinical trials. TMEM16A inhibitors, such as MONNA, Ani9, and 2-acylaminocycloalkylthiophene derivatives, have been also identified and represent tools of research to assess the role of TMEM16A in different organs and tissues. Overall, the efforts towards the development of modulators of alternative ion channels and transporters opens new avenues for improving mucociliary clearance in CF. - Source: PubMed
Publication date: 2025/10/31
Lipani AlessandraMascolo Fabiana LoGiuffrida StefanoBarreca MariliaBivacqua RobertaSpanò VirginiaRaimondi Maria ValeriaBorrelli AnnaVenturini AriannaGuidone DanielaGenovese MicheleMontalbano AlessandraGalietta Luis J VBarraja Paola