Ask about this productRelated genes to: SLC7A5 antibody
- Gene:
- SLC7A5 NIH gene
- Name:
- solute carrier family 7 member 5
- Previous symbol:
- -
- Synonyms:
- LAT1, E16, D16S469E, MPE16, CD98
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-28
- Date modifiied:
- 2016-10-05
Related products to: SLC7A5 antibody
Related articles to: SLC7A5 antibody
- Targeted delivery systems offer a promising approach for selectively modulating cellular processes; yet the intracellular consequences of targeted nutrient delivery to trophoblast cells remain poorly defined. Here, we investigated a previously validated placenta-targeting peptide conjugated to liposomes encapsulating stable isotope-labelled L-arginine and L-lysine to examine cellular uptake and downstream molecular responses in a trophoblast-like cell model. Peptide-dependent uptake of fluorescently labelled liposomes was confirmed in BeWo cells, demonstrating selective internalisation compared with non-targeted controls. Encapsulation of isotope-labelled amino acids enabled direct quantification of intracellular delivery and incorporation into the cellular proteome using stable isotope labelling by amino acids in cell culture (SILAC). Quantitative proteomic analysis revealed coordinated changes in proteins associated with translation, metabolism, and nitric oxide synthase regulation following targeted liposomal uptake. Notably, V-type proton ATPase subunit G1 (ATP6V1G1) and large neutral amino acid transporter small subunit 1 (SLC7A5) showed increased incorporation of labelled amino acids and were independently validated by Western blotting. Together, these findings establish a proof-of-concept platform for targeted intracellular amino acid delivery to trophoblast-like cells and define the resulting proteomic responses. This work provides mechanistic insight into intracellular amino acid utilisation and a framework for future studies in placental cell biology. - Source: PubMed
Publication date: 2026/04/23
Mazey EmilyFlannery SarahFischer RomanKandzija NevaZhang WeiYamada YumaTokeshi ManabuJohnson ErrinAkbar NaveedBancroft JamesHannan Fadil MVatish Manu - Acute mountain sickness (AMS) arises from hypobaric hypoxia at high altitude and still lacks effective pharmacological treatments. Although hypoxic preconditioning via gradual ascent prevents AMS, the underlying molecular adaptations have not yielded therapeutics. Here, inspired by metabolic reprogramming during stepwise altitude adaptation, we screened for anti-hypoxia compounds and identified H0802 (N-(pyridin-2-yl) pyridine-2-carbothioamide) as the most promising candidate. H0802 markedly enhances hypoxic tolerance in mice, prolongs survival under acute hypoxia, improves survival during simulated high-altitude exposure, and attenuates hypoxia-induced lung injury, accompanied by combined anti-inflammatory and antioxidant effects. Transcriptomic profiling shows that H0802 elicits a gene expression signature resembling hypoxia, including key hypoxia-related genes (, , , , , and ) involved in glucose and oxygen metabolism. Mechanistically, H0802 stabilizes endogenous hypoxia-inducible factor (HIF) proteins under normoxia by preventing ubiquitin-dependent degradation, thereby activating hypoxia-responsive genes. In vivo, H0802 pretreatment lowers circulating glucose and hepatic glycogen while increasing brain glucose uptake, suggesting a metabolic shift that preserves cerebral energy during acute hypoxic stress; it also modulates whole-body oxygen consumption. H0802 represents a candidate for anti-AMS therapy, and phenotypic optimization of H0802 provides a potential route for drug discovery. - Source: PubMed
Publication date: 2026/04/22
Yin LehuaLiu ZhehanLi YiranLi LeiLi XihengYang XingxingZhang JinyanHuang ShaoyiSun HaoYan XuHe WeihuiZhang ShaoyuGao JianqinChen JiaLiu YaohuiHan QiuyingZhou TaoHe XinhuaChen Yuan - Heat stress (HS) is among the most economically consequential environmental challenges to global dairy production, causing progressive declines in milk yield, compositional quality, and mammary cellular integrity. The temperature-humidity index (THI) is the primary thermal load metric, with performance-impairment thresholds typically beginning at THI 68 in Holstein cattle, with severe impacts manifesting beyond THI 72; breed-specific thresholds for Jersey, Brown Swiss, and Simmental cows differ owing to their lower metabolic heat load and greater inherent thermotolerance. At the molecular level, HS activates heat shock protein networks-notably , , and -through / transcriptional activation, while simultaneously suppressing casein genes (, , ), lipogenic genes (, , ), amino acid transporters (, ), and mTOR-AKT-STAT5 translational machinery, collectively impairing milk biosynthetic capacity. Pro-apoptotic signaling (, upregulation; downregulation) and mitochondrial dysfunction further compromise mammary epithelial viability. Post-transcriptional regulation through miRNA, circRNA, and lncRNA competing endogenous RNA networks, alongside epitranscriptomic m6A modifications, adds further regulatory complexity. Genome-wide association studies have identified SNPs in , , , and as thermotolerance candidates compatible with sustained milk production. Nutritional supplementation with methionine, arginine, and taurine partially restores cellular synthetic capacity. Integrating multi-trait genomic selection with introgression, precision cooling, and targeted nutrition offers the most viable path toward climate-resilient, high-producing dairy cattle. - Source: PubMed
Publication date: 2026/05/21
Ma QingshanTharwat MohamedAlshanbari Fahad AKhan Muhammad Zahoor - Left ventricular hypertrophy (LVH) is a major complication of chronic hypertension and an independent risk factor for cardiovascular morbidity and mortality. There are currently no clinically validated markers available to identify hypertensive individuals at risk for developing LVH. In hearts of hypertensive rats, we previously described metabolic changes that precede LVH development, including in branched-chain amino acid (BCAA) metabolism. This study investigated whether cardiac leucine uptake, measured with dynamic 5-[ F]fluoroleucine positron emission tomography-computed tomography ([ F]FLE-PET/CT), was impaired and could serve as an marker for hypertension-induced LVH development. - Source: PubMed
Publication date: 2026/05/14
Terrell WilliamLi JieKommi Damodara NBurt MeganJansen Maurits AKhanapur ShivashankarKeller Susanna RKundu Bijoy - Heavy metal contamination has become an emerging global health concern, yet the promoting effects of mixed heavy metal exposure on colorectal cancer risk remains poorly understood. In this study, plasma concentrations of 25 heavy metals were obtained from an in-house elemental database comprising both colorectal cancer patients and healthy controls, and exposure concentrations were then defined based on these human plasma detection data and relevant public datasets. Machine learning algorithms and mixture exposure models were applied to identify key heavy metals associated with colorectal cancer risk. RNA-seq datasets were integrated to screen for genes exhibiting heavy metal-tumor-specific characteristics. A total of 270379 cells from 95 samples were analyzed to identify cell subsets sensitive to mixed heavy metal exposure. Molecular and cellular experiments were performed to validate the underlying mechanisms. We first identified stannum (Sn), antimony (Sb), tantalum (Ta), and thallium (Tl) as a mixture of heavy metal highly associated with colorectal cancer risk. , and were further identified as key genes linked to colorectal tumors under conditions of mixed heavy metal exposure. Based on scRNA-seq analyses, endothelial tip cells were first identified as exhibiting heightened sensitivity to mixed heavy metal exposure. Mechanistically, acute mixed heavy metal exposure upregulated VEGFA expression in colorectal tumor epithelial cells. Co-culture experiments demonstrated enhanced epithelial-endothelial communication through the VEGFA-FLT1 axis, accompanied by increased expression of ESM1 and ANGPT2 in endothelial cells. Collectively, these findings suggest that mixed heavy metal exposure promotes angiogenesis by enhancing the interaction between colorectal tumor epithelial and endothelial cells, thereby increasing the risk of colorectal cancer. This study provides a scientific basis for improving strategies to control heavy metal contamination. - Source: PubMed
Publication date: 2026/05/25
Zhang ShuoZheng YudanWang JingZhou JieyuLi ZhengyiZhou ZiyanXu ShenyaXin JunyiFu ZanGu DongyingLi ShuweiWang Meilin