Ask about this productRelated genes to: SLC5A10 antibody
- Gene:
- SLC5A10 NIH gene
- Name:
- solute carrier family 5 member 10
- Previous symbol:
- -
- Synonyms:
- SGLT5
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2016-02-17
Related products to: SLC5A10 antibody
Related articles to: SLC5A10 antibody
- As a downstream product of transcriptional regulation, mRNA offers valuable insights into age-associated molecular changes and shows considerable potential for applications in age estimation. In this study, RNA sequencing was conducted on peripheral blood samples from 127 healthy Chinese individuals spanning a broad age range (18-80 years). Differential expression analysis were performed on expression profiles among the young (＜30 years), middle-aged (30-60 years) and elderly (＞60 years) groups. A total of 79 differentially expressed genes (DEGs) were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analysis revealed that the DEGs were mainly involved in response to type I interferon and cell-cell adhesion, which may reflect the activation of pro-inflammatory responses and neurodegenerative changes associated with aging. Through Spearman correlation analysis and the Lasso regression method, 34 candidate age-related genes (ARGs) were selected as predictive features. Notably, seven of these mRNAs (ARHGEF4, ARF6, AMIGO1, FITM2, PLEKHG4, SLC5A10, and HKR1) were identified for the first time as ARGs. Age prediction models were then constructed using five machine learning algorithms, with a 7:3 split for the train set and test set. Internal validation was conducted using 20 samples from the same cohort, while external validation was performed using two independent datasets: GSE262619 and GSE124326. Among them, the elastic net model showed the best performance, yielding a mean absolute error (MAE) of 6.72 years on the test set, 7.56 years on the internal validation set and 11.74 years on the external validation set, demonstrating strong robustness in age prediction. In general, this study delineated age-associated mRNA expression patterns and established a robust and accurate age prediction model based on a minimal set of 34 mRNA markers. - Source: PubMed
Publication date: 2025/10/11
Liao MengxiaoChen AnqiXuan YujiaZhao JinyuanLiu SitongXing YuZhang SuhuaLi Chengtao - Epilepsy, affecting approximately 50 million individuals worldwide, exhibits a genetic heritability of 32%. While several genes/loci associated with epilepsy have been identified through candidate and genome-wide association studies (GWAS), exploration of population-specific markers remains underexplored. We conducted the first GWAS in north Indian population (~1500 samples) to identify genetic variants/loci associated with epilepsy risk, validated using targeted next-generation sequencing (NGS). Our GWAS revealed 30 variants across seven loci associated with epilepsy risk, including six novel loci. Subtype analysis based on etiology and seizure types, identified 57 variants across 11 loci, 10 of which are novel. Gene-set analysis unveiled enrichment in genes associated with glutathione synthesis and recycling and regulation of dopaminergic neuron differentiation pivotal in epilepsy pathophysiology. Furthermore, PRS analysis revealed a significant genetic contribution to the epilepsy with an R of 0.00573. Additionally, targeted NGS showed ~95% concordance with GSA genotypes. Our study highlights six novel loci rs17031055/4q31.3(DCHS2), rs73182224/3q27.2(DGKG), rs9322462/6q25.2(CNKSR3), rs75328617/8q24.23(RNU1-35P), rs2938010/10q26.13(CTBP2) and rs11652575/17p11.2(SLC5A10) associated with epilepsy risk. These findings offer valuable insights into the genetic landscape of epilepsy in the north Indian population, providing foundation for future exploratory studies. - Source: PubMed
Publication date: 2025/02/04
Thakran SaritaGuin DebleenaSingh PriyankaUppili BharathramRamachandran SrinivasanKushwaha Suman SKukreti Ritushree - Excessive fructose intake causes a variety of adverse conditions (e.g., obesity, hepatic steatosis, insulin resistance and uric acid overproduction). High fructose-induced hypertension is a particularly common and pathologically significant condition induced by excess fructose, but its underlying mechanisms remain unknown. We investigated these mechanisms in 7-week-old male Sprague-Dawley rats fed normal rat food or a diet containing 60% glucose (GLU group) or 60% fructose (FRU group) for 3, 6, or 12 weeks. Daily food consumption was measured to avoid between-group discrepancies in caloric/salt intake, adjusting for feeding amounts. The mean blood pressure of FRU rats was significantly higher (12 weeks GLU: 94.8 ± 3.4 mmHg vs. 12 weeks FRU: 103.7 ± 1.2 mmHg), and fractional sodium excretion was significantly lower (12 weeks GLU: 0.084 ± 0.011% vs. 12 weeks FRU: 0.059 ± 0.08%), indicating that the high-fructose diet caused salt retention. The kidney weight and glomerular surface area were greater in FRU rats (12 weeks GLU: 7495 ± 181 vs. 12 weeks FRU: 9831 ± 164 μm), suggesting that the high-fructose diet induced an increase in extracellular fluid volume. The expressions of GLUT5 and ketohexokinase, an enzyme required for fructose metabolism, were up-regulated in the FRU group rats (GLUT5 12 weeks GLU: 104.7 ± 15.4% vs. 12 weeks FLU: 309.0 ± 99.9%, ketohexokinase 12 weeks GLU: 129.6 ± 3.5% vs. 12 weeks FLU: 163.9 ± 13.0%). Cortical ATP levels were significantly lower in FRU rats (12 weeks GLU: 9.82 ± 1.26 nmol/mg protein vs. 12 weeks FRU: 7.59 ± 1.68 nmol/mg protein), possibly indicating ATP consumption due to fructose metabolism. Unlike in previous reports the high-fructose diet did not affect NHE3 expression (12 weeks GLU: 166.1 ± 6.3% vs. 12 weeks FLU: 142.0 ± 5.9%). A gene chip analysis conducted to identify susceptible molecules revealed that only Slc5a10 (corresponding to SGLT5) showed >two-fold up-regulation in FRU versus GLU rats. RT-PCR and in situ hybridization confirmed the SGLT5 up-regulation (12 weeks GLU: 75.0 ± 5.8% vs. 12 weeks FLU: 230.1 ± 16.0%). Our findings may indicate that the high-fructose diet increased sodium reabsorption principally through up-regulated SGLT5, finally causing salt-sensitive hypertension. - Source: PubMed
Publication date: 2024/12/20
Hara HiroakiTakayanagi KaoriShimizu TaisukeIwashita TakatsuguIkari AkiraMaeshima AkitoHasegawa Hajime - Considering the age relevance of prostate cancer (PCa) and the involvement of the cGAS-STING pathway in aging and cancer, we aim to classify PCa into distinct molecular subtypes and identify key genes from the novel perspective of the cGAS-STING pathway. It is of significance to guide personalized intervention of cancer-targeting therapy based on genetic evidence. - Source: PubMed
Publication date: 2024/06/14
Yang JieXu ZihanZheng WeitaoLi YifanWei QiangYang Lu - The European-centered genome-wide association studies of schizophrenia (SCZ) may not be well applied to non-European populations. We analyzed 1,592 reported SCZ-associated genes using the public genome data and found an overall higher Asian-European differentiation on the SCZ-associated variants than at the genome-wide level. Notable examples included 15 missense variants, a regulatory variant -rs1624825, and a damaging variant -rs1001292. Independent local adaptations in recent 25,000 years, after the Asian-European divergence, could have contributed to such genetic differentiation, as were identified at a missense mutation -rs57646126-A in Asians, and a non-risk allele -rs72761442-G in Europeans. Altai-Neanderthal-derived alleles may have opposite effects on SCZ susceptibility between ancestries. Furthermore, adaptive introgression was detected on the non-risk haplotype at 1q21.2 in Europeans, while in Asians it was observed on the SCZ risk haplotype at 3p21.31 which is also potentially ultra-violet protective. This study emphasizes the importance of including more representative Asian samples in future SCZ studies. - Source: PubMed
Publication date: 2024/03/26
Chen SihanTang DieDeng LianXu Shuhua