Ask about this productRelated genes to: SLC22A13 Blocking Peptide
- Gene:
- SLC22A13 NIH gene
- Name:
- solute carrier family 22 member 13
- Previous symbol:
- ORCTL3
- Synonyms:
- OCTL1, OCTL3, OAT10
- Chromosome:
- 3p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-31
- Date modifiied:
- 2016-02-18
Related products to: SLC22A13 Blocking Peptide
Related articles to: SLC22A13 Blocking Peptide
- Carrier-mediated uptake of choline is rate-limiting for acetylcholine biosynthesis and various other biological processes. To date, 16 solute carrier (SLC) proteins have been identified that may facilitate choline permeation across the outer cell membrane. However, their biochemical functions have not yet been experimentally compared. We overexpressed 16 SLC proteins with known choline-transporting capacity and compared their choline transport kinetics. Additionally, we evaluated their capacity to transport choline analogues as well as metabolites involved in its biosynthesis and degradation or modulators of cholinergic neurotransmission to gain insight into the biological functions of the SLCs. Furthermore, we investigated whether the transporters could be distinguished by their sensitivity to inhibition by hemicholinium-3 and other substances. Of the 16 SLCs tested, seven (SLC5A7, SLC35F2, SLC35F3, SLC35F4, SLC25F5, SLC35G4, and SLC44A5) exhibited K values for choline transport in the range of 12 to 50 µM, closely aligning with physiological plasma choline concentrations. Among them, SLC5A7 displayed over tenfold higher intrinsic clearance than any of the others. SLC22A1-3 were confirmed as choline transporters, albeit with low affinity. Hemicholinium-3 most strongly inhibited SLC5A7 and also significantly inhibited SLC35F2-5 and SLC35G4. Choline transport by these six transporters was inhibited by about 50 % at 100 µM decynium-22 and verapamil.. In humans, multiple SLCs may contribute to cellular choline uptake, depending on physiologic conditions and their yet incompletely characterized expression patterns. The present data may also enhance our understanding of inherited and environmental modulation of these transporters with possible consequence, for instance, on motor and cognitive functions. - Source: PubMed
Publication date: 2025/09/17
Redeker Kyra-Elisa MariaBrockmöller Jürgen - IgA nephropathy represents a significant challenge in nephrology research, and an understanding of its underlying molecular mechanisms is crucial. In this study, we conducted a comprehensive proteomic investigation of IgA nephropathy utilizing microdissection techniques combined with data-independent acquisition technology. Our analysis focused on differentially expressed proteins in the glomeruli, interstitium, and tubules of the kidney. Functional enrichment analysis revealed distinct pathway enrichment patterns, with fatty acid synthesis predominating in the glomerulus and complement and coagulation pathways predominantly enriched in the tubules. These pathway enrichments suggest potential key contributors to the pathogenesis of IgA nephropathy. Furthermore, our study identified ATP1B1 and COX4I1 in the glomerulus and SLC22A13 in the tubules as promising diagnostic markers for the disease. Meanwhile, C4A and APEX1 proteins were identified as valuable biomarkers for assessing disease progression. This research could provide valuable insights into the proteomic alterations associated with IgA nephropathy and offer potential targets for further therapeutic exploration. - Source: PubMed
Publication date: 2025/04/24
Huang JingxianZhu HongguoLi ShanshanQiu JingYang HougangZheng FengpingLuo ZhifengYan QiangLiu FannaYin LianghongTang DongeDai Yong - To summarize the effects of single nucleotide polymorphisms (SNPs) on the pharmacokinetics of allopurinol to control uric acid levels. A comprehensive search was conducted in PubMed, Web of Science and Scopus databases from inception to January 2024, includes 17 articles focusing on SNPs and pharmacokinetics of allopurinol and oxypurinol. A total of 11 SNPs showed a significant association with pharmacokinetics of allopurinol and oxypurinol, as well as their potential clinical implications. SNPs in ATP-binding cassette super-family G member 2 (), solute carrier family 2 member 9 (), solute carrier family 17 member 1 (), solute carrier family 22 member 12 (), solute carrier family 22 member 13 () and PDZ domain containing 1 () genes were associated with allopurinol clearance, while SNPs in aldehyde oxidase 1 () genes involved in metabolism of allopurinol. SNPs in gremlin 2, DAN family BMP antagonist () gene impacted uric acid control, but the specific mechanism governing the expression of remains unknown. Our study indicated that the identified SNPs show contradictory effects, reflecting inconsistencies and differences observed across various studies. - Source: PubMed
Publication date: 2024/09/30
A Zairol Azwan Farah AidaTeo Yi YingMohd Tahir Nor AsyikinSaffian Shamin MohdMakmor-Bakry MohdMohamed Said Mohd Shahrir - Genetic variations in urate transporters play a significant role in determining human urate levels and have been implicated in developing hyperuricemia or gout. Polymorphism in the key urate transporters, such as ABCG2, URAT1, or GLUT9 was well-documented in the literature. Therefore in this study, our objective was to determine the frequency and effect of rare nonsynonymous allelic variants of , , and on urate transport. In a cohort of 150 Czech patients with primary hyperuricemia and gout, we examined all coding regions and exon-intron boundaries of , , and using PCR amplification and Sanger sequencing. For comparison, we used a control group consisting of 115 normouricemic subjects. To examine the effects of the rare allelic nonsynonymous variants on the expression, intracellular processing, and urate transporter protein function, we performed a functional characterization using the HEK293A cell line, immunoblotting, fluorescent microscopy, and site directed mutagenesis for preparing variants . Variants p.V202M (rs201209258), p.R343L (rs75933978), and p.P519L (rs144573306) were identified in the gene (OAT4 transporter); variants p.R16H (rs72542450), and p.R102H (rs113229654) in the gene (OAT10 transporter); and the p.W75C variant in the gene (NPT1 transporter). All variants minimally affected protein levels and cytoplasmic/plasma membrane localization. The functional assay revealed that contrary to the native proteins, variants p.P519L in OAT4 ( ≤ 0.05), p.R16H in OAT10 ( ≤ 0.05), and p.W75C in the NPT1 transporter ( ≤ 0.01) significantly limited urate transport activity. Our findings contribute to a better understanding of (1) the risk of urate transporter-related hyperuricemia/gout and (2) uric acid handling in the kidneys. - Source: PubMed
Publication date: 2024/01/06
Vávra JiříPavelcová KateřinaMašínová JanaHasíková LenkaBubeníková EliškaUrbanová AnetaMančíková AndreaStibůrková Blanka - (1) Background: Many transporters of the SLC22 family (e.g., OAT1, OAT3, OCT2, URAT1, and OCTN2) are highly expressed in the kidney. They transport drugs, metabolites, signaling molecules, antioxidants, nutrients, and gut microbiome products. According to the Remote Sensing and Signaling Theory, SLC22 transporters play a critical role in small molecule communication between organelles, cells and organs as well as between the body and the gut microbiome. This raises the question about the potential role of SLC22 transporters in cancer biology and treatment. (2) Results: In two renal cell carcinoma RNA-seq datasets found in TCGA, KIRC and KIRP, there were multiple differentially expressed (DE) SLC22 transporter genes compared to normal kidney. These included SLC22A6, SLC22A7, SLC22A8, SLC22A12, and SLC22A13. The patients with disease had an association between overall survival and expression for most of these DE genes. In KIRC, the stratification of patient data by pathological tumor characteristics revealed the importance of SLC22A2, SLC22A6, and SLC22A12 in disease progression. Interaction networks combining the SLC22 with ADME genes supported the centrality of SLC22 transporters and other transporters (ABCG2, SLC47A1) in disease progression. (3) Implications: The fact that many of these genes are uric acid transporters is interesting because altered uric acid levels have been associated with kidney cancer. Moreover, these genes play key roles in processing metabolites and chemotherapeutic compounds, thus making them potential therapeutic targets. Finally, our analyses raise the possibility that current approaches may undertreat certain kidney cancer patients with low SLC22 expression and only localized disease while possibly overtreating more advanced disease in patients with higher SLC22 expression. Clinical studies are needed to investigate these possibilities. - Source: PubMed
Publication date: 2022/09/29
Whisenant Thomas CNigam Sanjay K