SLC7A9 Antibody
- Known as:
- SLC7A9 Antibody
- Catalog number:
- XW-8130
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC7A9 Antibody
Related genes to: SLC7A9 Antibody
- Gene:
- SLC7A9 NIH gene
- Name:
- solute carrier family 7 member 9
- Previous symbol:
- CSNU3
- Synonyms:
- -
- Chromosome:
- 19q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-16
- Date modifiied:
- 2016-02-17
Related products to: SLC7A9 Antibody
Related articles to: SLC7A9 Antibody
- : Cystinuria is an inherited disorder characterized by impaired proximal tubular reabsorption of cystine, resulting in recurrent cystine stone formation. Mutations in the and genes are the main genetic causes of the disease, while variants in have also been associated with cystinuria in specific populations. Despite advances in understanding its molecular basis, cystinuria remains clinically heterogeneous, making disease progression and prognosis difficult to predict. This study aimed to investigate circulating microRNAs (miRNAs) as potential molecular biomarkers, characterize their expression profile in patients with cystinuria, and evaluate their association with clinical indicators of disease severity. : The study group included 16 patients with a clinically established diagnosis of cystinuria, while the control group consisted of 11 healthy individuals without a history of nephrolithiasis. Candidate miRNAs were selected based on their predicted regulatory interactions with genes implicated in cystinuria pathogenesis. Eight microRNAs (miR-29a-3p, miR-29b-3p, miR-29c-3p, miR-1207-3p, miR-10a-3p, miR-3658, miR-141-3p, and miR-200a-3p) were analyzed by quantitative real-time PCR (qPCR). Among the eight miRNAs evaluated, miR-10a, miR-141, miR-200a, and miR-3658 were significantly downregulated in patients with cystinuria compared with healthy controls. Higher expression levels of miR-10a, miR-141, and miR-200a were significantly associated with a greater number of previous surgical procedures ( < 0.05). Additionally, increased miR-10a expression was associated with impaired renal function, defined as serum creatinine levels above 1.2 mg/dL. miR-10a, miR-141, miR-200a, and miR-3658 were significantly downregulated in patients with cystinuria compared with healthy controls. Within the cystinuria cohort, higher expression of miR-10a was associated with impaired renal function, whereas increased expression of miR-10a, miR-141, and miR-200a correlated with a greater number of surgical interventions, suggesting a potential relationship with disease severity. Further studies in larger, genetically characterized cohorts are warranted to clarify the biological role and clinical utility of these miRNAs as biomarkers of cystinuria. - Source: PubMed
Publication date: 2026/07/28
Ayres Daniel CernachPimenta RuanDos Santos Gabriel ArantesCandido PatríciaAntunes MilenaDip Junior Nelson GasparMarchini Giovanni STorricelli Fábio CVicentini Fábio CDanilovic AlexandreBatagello Carlos ALeite Kátia R MNahas William CReis Sabrina TMazzucchi Eduardo - Cystinuria is a rare inherited disease characterized by increased urinary cystine levels resulting in the formation of cystine stones in the urinary tract. Mutations in the genes encoding the cystine transporter complex, SLC3A1 and SLC7A9, are the primary drivers of the disease. Current mouse models used to study cystinuria rely on gene deficiency or spontaneous mutations in mice that do not accurately reflect the pathogenic mutations found in humans. - Source: PubMed
Publication date: 2026/08/18
Bhatt Nirmal PNguyen Theresa T HIacono GiuliaRodriguez Gabriel RAnderson Connor R BPerry AndrewBarlow Christopher KAnderson DovileBurgio GaetanMarsland Benjamin JJiang Simon HDeshpande Aniruddh VStarkey Malcolm R - Cystine stones account for 1%‒2% of adult and up to 10% of pediatric kidney stones. They result from cystinuria, an autosomal recessive disorder caused by mutations in solute carrier family 3 member 1 () and , which encode the renal cystine transporter subunits. These mutations impair cystine reabsorption, raising urinary cystine levels and driving stone formation. Current diagnostic options remain limited in terms of detecting molecular dysfunctions. Thus, we aimed to develop a nonradioactive, cell-based method for the functional assessment of cystine transporters and mutation-specific pathologies. - Source: PubMed
He XiaobaiQian XinyiZheng XiaoguangZhang HongShao JinbangChen XiaopanRuan QiLyu JianxinYang LeixiangChen Linjie - Mutations of LDLR, APOB and PCSK9 have been well-established to cause hypercholesterolemia while the pathogenic effects of LPL has been confirmed by cohorts and functional studies in hypertriglyceridemia. However, these mutations do not fully account for all dyslipidemia, and it remains unexplained why some patients with dyslipidemia develop coronary heart disease (CHD) while others do not. - Source: PubMed
Publication date: 2026/05/12
Huang ManSong XiuliZhou ShuniZhang HaiyanHe LijuanChen YanghuiChen GuangzhiDing HuJiang JiangangWang YanWang Dao WenSun YangWang Hong - BACKGROUND: Prostate cancer (PCa) clinical management is challenged by tumor heterogeneity, driving the need for robust prognostic biomarkers, with altered glutamine metabolism emerging as a promising target. This investigation aimed to construct a metabolism-based prognostic signature for PCa and translate it into a targeted nanotherapeutic strategy. METHODS: Transcriptomic data from The Cancer Genome Atlas (TCGA) were analyzed to identify dysregulated glutamine metabolism genes and construct a prognostic model via univariate Cox, LASSO, and multivariate Cox regression with validation in an independent cohort. The model’s characteristics were assessed through tumor microenvironment (TME), tumor mutation burden (TMB), and consensus clustering analyses. The pivotal gene of the model was selected to functionally validate in vitro through proliferation, clonogenicity, migration, and invasion assays. To exploit this vulnerability, a CB/CDDP@lipo nanoplatform was engineered to co-deliver cisplatin and glutaminase inhibitor CB-839, with evaluation in PCa models in vitro and in vivo. RESULTS: A novel five-gene prognostic signature (ASNS, ATP2B4, GLYATL1, SLC6A20, SLC7A9) was established and stratified PCa patients into high- and low-risk groups based on progression-free interval (PFI). High-risk patients exhibited an immunosuppressive TME, higher TMB and TP53 mutations, and activation of proliferation-related pathways. Functional validation identified ASNS as a key oncogenic driver, enhancing PCa tumor cell proliferation, migration, and invasion. Therapeutically, CB/CDDP@lipo nanoplatform demonstrated potent synergistic cytotoxicity by depleting glutathione (GSH) and amplifying oxidative stress. This dual-action mechanism triggered significant apoptosis and tumor suppression with a favorable safety profile. CONCLUSIONS: Our study establishes a glutamine metabolism-based prognostic signature, pinpointing ASNS as a key driver. The resulting CB/CDDP@lipo nanoplatform offers a promising chemo-metabolic strategy for enhanced PCa treatment. - Source: PubMed
Publication date: 2026/04/18
Li WenyaGe WeiyingNi WenjieZhang HaoGuo YangyangXie YuxinZhou ZhenLi YimingZheng ZheLi JianminZhao Yang