Ask about this productRelated genes to: SLC34A3 antibody
- Gene:
- SLC34A3 NIH gene
- Name:
- solute carrier family 34 member 3
- Previous symbol:
- -
- Synonyms:
- NPTIIc, FLJ38680
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-08-08
- Date modifiied:
- 2016-02-17
Related products to: SLC34A3 antibody
Related articles to: SLC34A3 antibody
- Calcium-phosphorus metabolism is critical for skeletal development in weaned piglets. This study evaluated the effects of dietary 25-hydroxyvitamin D (25-OH-VD) in combination with phytase and probiotics on mineral metabolism, bone development, and related molecular mechanisms in weaned piglets. Sixty 28-day-old weaned piglets (7.1 ± 1.30 kg) were randomly assigned to four dietary treatments for 31 days (including 3 days of acclimation): CON (basal diet + 50 µg/kg 25-OH-VD), HI (CON + 50 mg/kg phytase), CY (CON +10 mg/kg probiotics), HICY (CON + 50 mg/kg phytase + 10 mg/kg probiotics). Apparent calcium digestibility, serum biochemical indices, bone mineral density (BMD), and mRNA and protein expression of calcium-phosphorus transport- and metabolism-related genes in jejunal mucosa and kidney were assessed. Compared with CON, piglets in the HI, CY, and HICY groups showed higher apparent calcium digestibility ( < 0.05). Serum transforming growth factor-β was elevated in CY and HICY ( < 0.05). HI enhanced metatarsal and toe BMD ( < 0.05) and upregulated jejunal solute carrier family 34, member 2 () and mRNA expression ( < 0.05). In contrast, HICY reduced mRNA expression of transient receptor potential cation channel subfamily V member 6 and calcium-binding protein D28k, as well as of and in the kidney ( < 0.05). Renal calcium-sensing receptor protein abundance increased in CY ( < 0.05). Supplementation of 25-OH-VD with phytase and/or probiotics improved calcium utilization and modulated key transport pathways, contributing to enhanced bone development in weaned piglets. These findings highlight coordinated nutritional regulation of mineral metabolism during early post-weaning growth. - Source: PubMed
Publication date: 2026/04/30
Shi BaoshiGong SaimingWang JingjingXi YuyueTang ZhiruGao JingchunXu YetongSun Zhihong - Peritoneal dialysis (PD) is limited by insufficient phosphate removal, leading to adverse cardiovascular outcomes in patients with chronic kidney disease. To advance the understanding of the molecular mechanisms of peritoneal phosphate transport, RNAseq data of phosphate transporters in four PD-relevant cell lines were analyzed. The expression and localization of the respective proteins were validated by immunostaining in these cells. The transcriptomics of omental arterioles from children on PD were analyzed. In vitro Transwell models of an immortalized mesothelial cell line (MeT-5A) and human umbilical vein endothelial cells (HUVECs) and respective co-cultures were established, enabling quantification of phosphate transport across mesothelial and endothelial monolayers. Sodium phosphonoformate tribasic hexahydrate (PFA) and Tenapanor were used to inhibit transcellular and paracellular transport pathways. Cell viability and integrity markers were measured over the experimental periods. and were expressed across all studied cell types, while and were mesothelial cell-specific. Omental arterioles of children on low-glucose-degradation-product (GDP) PD showed higher expression vs. stage 5 chronic kidney disease (CKD5) and healthy controls. Permeability for phosphate was lower across MeT-5A compared with HUVEC monolayers and was not further reduced in co-culture. Inhibitors reduced both transcellular and paracellular transport to 75% in MeT-5A and 65% in co-cultures, while no effects were observed in HUVEC alone, suggesting the mesothelial cell layer as a significant barrier for phosphate transport. Our studies provide first analyses combining findings on molecular phosphate transporters in peritoneal cells and arterioles and introducing a Transwell model for quantitative studies of phosphate kinetics. - Source: PubMed
Publication date: 2026/04/21
Du ZhiweiBartosova Medvid MariaMarinovic IvaZarogiannis Sotirios GSchmitt Claus Peter - Renal Fanconi syndrome (RFS) refers to a generalized dysfunction of the proximal tubule, including impaired 1-α hydroxylation of vitamin D. Consequently, rickets is a typical complication. Clinical observations in children with severe nutritional vitamin D deficiency sometimes include proximal tubular dysfunction, raising the possibility that lack of vitamin D could not only be a consequence of RFS but also a cause of it, although this has never been confirmed. Observations in Mendelian disorders with their genetically defined pathophysiology can provide clearer insights. - Source: PubMed
Publication date: 2026/05/02
Zerrouki SamiaSoyalp GonencTaillandier LucieHamida KarimBendib SchahrazedBensid IkramChelih SabrinaMekahli DjalilaBockenhauer Detlef - Kidney stones are common and can arise from many etiologies including genetic and environmental. Biallelic pathogenic variants in the solute carrier family 34-member 3 (SLC34A3) gene cause Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH), while both monallaelic and biallelic pathogenic variants in SLC3A1 cause cystinuria. Here, we report the clinical phenotype of a patient with concomitant biallelic and monoallelic pathogenic variants in SLC34A3 and SLC3A1 respectively. - Source: PubMed
Publication date: 2026/03/18
Olarewaju Bukola ASabrowsky SoniaShurrab ShaymaaMoyer Ann MKeddis Mira TOsundiji Mayowa A - Medullary sponge kidney (MSK) is characterized by precalyceal dilatation of the renal tubules. This entity is associated with recurrent kidney stone disease (KSD). Although etiopathogenesis is unknown, genetic origin is suspected. - Source: PubMed
Publication date: 2026/03/06
Tournebize CorentinRobert ThomasAbid NadiaDe Mul AurélieSchleef MaximeLefevre FloraDubourg LaurenceDancer MarineLetavernier EmmanuelLemoine Sandrine