Ask about this productRelated genes to: SLC5A3 antibody
- Gene:
- SLC5A3 NIH gene
- Name:
- solute carrier family 5 member 3
- Previous symbol:
- -
- Synonyms:
- SMIT, SMIT1
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-15
- Date modifiied:
- 2016-02-17
Related products to: SLC5A3 antibody
Related articles to: SLC5A3 antibody
- Hyperlipidemia refers to the abnormal elevation in the levels of one or more plasma lipids and lipoproteins. - Source: PubMed
Publication date: 2026/04/09
Alwahsh MohammadAlejel RahafHamadneh LamaHasan AyaAl-Hiari YusufAl-Qirim TariqHergenröder Roland - Neurons and glial cells are biochemically coupled through the exchange of nutrients, but our knowledge of which metabolites are transferred between them remains limited due to technical challenges. Here, we introduce a strategy to label specific cell types with isotopic tracers so that metabolite transfer can be measured directly in the intact brain. By engineering neurons in mice to metabolize C-labeled cellobiose, a glucose dimer that wild-type cells cannot catabolize, we selectively track neuron-derived metabolites by using mass spectrometry-based metabolomics. Applying this approach enabled us to identify -inositol as a critical metabolite synthesized by neurons and transferred to oligodendrocyte progenitor cells (OPCs) via the SLC5A3 transporter. The transfer of -inositol from neurons to OPCs promotes OPC proliferation and differentiation by enhancing phosphatidylinositol synthesis and upregulating expression of myelin-associated genes. During demyelination, deficient nutrient transfer can be rescued by dietary supplementation of -inositol, which accelerates myelin repair. These findings establish a generalizable technology for tracing intercellular metabolite transfer and identify a previously unrecognized mechanism of -inositol transfer from neurons to glial cells in support of CNS regeneration, revealing a potential metabolic target for therapeutic intervention in neurodegenerative disease. - Source: PubMed
Publication date: 2026/03/22
Adkins-Travis KaylaSong Mun-GuSchwaiger-Haber MichaelaCho KevinFowle-Grider RonaldJohnson Stephen LShriver Leah PPatti Gary J - Recent clinical studies have reported that myo-inositol is consistently elevated in plasma of patients with heart failure (HF), yet its role in cardiac dysfunction remains poorly understood. Myo-inositol is specifically transported into cells by the sodium-myo-inositol co-transporter-1 (SMIT1), a member of the sodium-glucose co-transporter (SGLT) family expressed in the heart. While myo-inositol is essential for phosphoinositide signalling, osmoregulation, and metabolic homeostasis, dysregulation of SMIT1-mediated myo-inositol transport may contribute to key pathological mechanisms in HF. This study aims to elucidate the role of SMIT1 in the failing heart, especially during left ventricular remodelling that precedes it. - Source: PubMed
Marino AliceCumps JulienGuilbert LauraGeiser AngélineBaufays ClaireGinion AudreyFerté LauraBattault SylvainDe Matos FionaAmbroise JeromeZuurbier Coert JLezoualc'h FrankPestiaux CamillePyka GrzegorzKerckhofs GreetRoderick H LlewelynBertrand LucHorman SandrineBeauloye Christophe - Macrophages play a key role in hepatocellular carcinoma (HCC) progression, but the mechanisms underlying this involvement remain unclear. In the present study, mice with HCC were used for experiments, and 97H and THP‑1 cells were used for experiments. Metabolomic analysis was performed to detect changes of metabolites in the supernatant of 97H cells. Flow cytometry and immunohistochemical staining were performed to assess macrophage polarization. Western blotting was performed to examine the levels of phosphorylated (p‑) PI3K, p‑AKT and NRF2. Reverse transcription‑quantitative polymerase chain reaction was performed to examine , and mRNA expression levels. FBXO22 significantly promoted the release of myo‑inositol in the cell supernatant of 97H cells, markedly decreased the number of CD86‑positive cells (M1 macrophages), and increased the number of CD206‑positive cells (M2 macrophages) in both THP‑1 cells and mouse HCC tumor tissues. The promoting effect of myo‑inositol on M2 macrophages was reversed by transfection with small interfering (si)‑SLC5A3 . In addition, FBXO22 overexpression reduced PTEN protein levels and then elevated NRF2 protein levels upregulating IMPA1 and inducing myo‑inositol release in 97H cells. Co‑culturing of 97H and THP‑1 cells revealed that the stimulatory effect of 97H cells transfected with an overexpression (oe)‑ construct on M2 macrophages was reversed by co‑transfection with the si‑. Co‑immunoprecipitation revealed a promoting effect of FBXO22 on PTEN ubiquitination via direct interaction in 97H cells. Furthermore, luciferase activity and chromatin immunoprecipitation assays indicated direct transcriptional regulation of IMPA1 expression by NRF2 in 97H cells. The experiments further revealed that transfection with the si‑ reversed the promoting effect of oe‑ on tumor growth and M2 polarization by reducing myo‑inositol levels in tumor tissues. In conclusion, FBXO22 degrades PTEN by inducing its ubiquitination to elevate NRF2 protein levels. As a result, IMPA1 expression is increased, which causes myo‑inositol release by HCC cells and further induces M2‑type macrophages via SLC5A3 to promote HCC tumor growth. The present study identified a novel molecular mechanism by which FBXO22 promotes HCC progression. - Source: PubMed
Publication date: 2025/12/05
Bai LiangliangXiong JingChen SihaiHu JiahaoZhang MeixiaLi BiminHu JingHe Mingyan - Gene discoveries in obesity have largely relied on homogeneous populations, limiting their generalizability across ancestries. Here, we conduct a gene-based rare variant association study of BMI on 839,110 individuals from six ancestries across two population-scale biobanks. A cross-ancestry meta-analysis identifies 13 genes, including YLPM1, RIF1, GIGYF1, SLC5A3, and GRM7, that confer about three-fold risk for severe obesity, are expressed in the brain and adipose tissue, and are linked to obesity traits such as body-fat percentage. While YLPM1, MC4R, and SLTM show consistent effects, GRM7 and APBA1 show significant ancestral heterogeneity. Polygenic risk additively increases obesity penetrance, and phenome-wide studies reveal additional associations, including YLPM1 with altered mental status. These genes also influence cardiometabolic comorbidities, including GIGYF1 and SLTM towards type 2 diabetes with or without BMI as a mediator, and altered levels of plasma proteins, such as LECT2 and NCAN, which in turn affect BMI. Our findings provide insights into the genetic basis of obesity and its related comorbidities across ancestries and ascertainments. - Source: PubMed
Publication date: 2025/10/30
Banerjee DeeproGirirajan Santhosh