SLC7A5 antibody
- Known as:
- SLC7A5 (anti-)
- Catalog number:
- orb77270
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SLC7A5 antibody
Related 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
- Mastitis in dairy cattle is a serious issue that affects not just the animals but also has broad social, cultural, economic, and human consequences. It does in a wide variety of ways and the most remarkable of which are reduced milk yield and produce poor milk quality. This study takes an approach of bioinformatics to track down new targets and biomarkers which can be used to diagnose the clinical and subclinical forms of mastitis and at the same time find the way to treat and manage the disease. Comparing genes that express at a different level and the protein network, we identified three key genes (CDKN1A, FKBP5 and SLC7A5) and pathways that mastitis includes both in clinical and subclinical form. In functional term, multicellular organismal process regulation, cell population proliferation, protein binding are identified as critical biological processes. Additionally, machine learning algorithms applied to validate the identified candidate biomarkers. Potential repurposing drug targets are identified based on the commonly selected differentially expressed genes. This integrative approach not only provides insights into the molecular mechanisms underlying mastitis but also offers a robust framework for developing targeted therapies and diagnostic tools, ultimately contributing to better herd health and productivity. The findings from this study pave the way for precision veterinary medicine, with the ability to decrease the impact of the economic burden of mastitis on the dairy industry. - Source: PubMed
Publication date: 2026/05/13
Auwul Md Rabiul - The aim of this study was to assess the effect of sertraline on the gene expression of placental transporters for hormones, folates, nutrients and drugs over the course of pregnancy in rats. The studies were conducted on gestational days (GDs) 16 and 20 following oral treatment with 10 mg/kg/day sertraline or the vehicle, administered from weaning onward. The weight and area of the fetuses and placentas were analyzed, and maternal plasma sertraline concentrations were measured. Gene expression of ATP-binding cassette transporter b1a and b1b ( and ), organic anion-transporting polypeptide 4a1(/), folate receptor-α (), reduced folate carrier (/), and L-type amino acid transporter (/) was evaluated in the placenta. Sertraline reduced fetal weight ( < 0.001) and fetal area ( < 0.01) at GD 16, while no significant differences were observed in placental weight or area between exposed and unexposed groups. Sertraline concentration was significantly lower at GD20 than at GD16 ( < 0.001). At GD 16, sertraline reduced the expression of ( = 0.027), ( < 0.01), and ( = 0.037) compared with controls. Conversely, sertraline induced expression in both GDs and increased expression at GD 20, while was not affected. These findings indicate that sertraline alters placental drug transporter gene expression and may impair nutrient transfer to the fetus. - Source: PubMed
Publication date: 2026/04/27
Enriquez-Mendiola DanielSifuentes-García Jorge EBarragán-Zúñiga Laura JVértiz-Hernández Angel ALazalde-Ramos Blanca PDamiano Alicia EGalaviz-Hernández CarlosSosa-Macías Martha - Idiopathic pulmonary fibrosis is a progressive and fatal disorder characterized by abnormal activation of alveolar fibroblasts. However, the metabolic reprogramming of alveolar fibroblasts during lung injury remains unclear. Here we show that uptake of branched-chain amino acids is increased, whereas their catabolism is significantly impaired in fibrotic lung fibroblasts and mouse lung tissues. Branched-chain amino acids promote lung fibroblast activation and bleomycin-induced lung fibrosis. Genetic inactivation of branched-chain amino acid transaminase 2 exacerbates fibrosis, whereas inhibition of the corresponding transporter SLC7A5 or enhancement of catabolism attenuates pulmonary fibrosis in male mice. Mechanistically, ATF4 and PPARγ regulate the expression of SLC7A5 and BCAA catabolic genes, respectively. We identify KDM4A as a key mediator of the epigenetic regulation of fibrotic genes. Notably, dysregulated BCAA metabolism is associated with disease severity in patients, suggesting that targeting BCAA metabolism may serve as a promising therapeutic strategy for idiopathic pulmonary fibrosis. - Source: PubMed
Publication date: 2026/04/27
Yao JieFang SuLei MiaoOu ZexianZeng ChuanfeiPeng WanliHe NaYang LianGuo BingpengFang MingmengWang CuihuaLv JieWu ShuangZhang Wei KevinHuang HuiminPeng YangRao WeiRong ZhiliYang PenghuiWang ChaoqunHan QianHu Wenxiang - Aging is characterized by changes in gut microbiome, metabolic imbalance and chronic inflammation, yet how these processes integrate to drive tissue degeneration remains poorly defined. Using age-related macular degeneration (AMD) as a model of tissue aging, we identify a diet-induced metabolic-immune axis that promotes systemic and retinal degeneration. In mice, a high-fat, cholesterol-enriched (HFC) diet induced perturbations in the gut structural integrity and microbiome repertoire, as well as systemic metabolic aging signatures, prominently marked by reduced circulating histidine. Plasma histidine levels were similarly decreased in AMD patients and inversely correlated with body mass index (BMI) in control donors. These diet-induced gut microbiome changes and subsequent metabolic alterations promoted peripheral innate immune reprogramming, with expansion of inflammatory neutrophils and monocytes that infiltrated the outer retina in a mouse model. Mechanistically, the gut-derived IGF1R/AKT2 signaling acts as a central regulator of global epigenetic remodeling and systemic immune aging under high-fat conditions in . In a mouse model with an age-dependent dry AMD-like pathology, distinct retinal pigment epithelium (RPE) subpopulations exhibited downregulation of the histidine transporter SLC7A5, linking metabolic stress to activation of MIF/CD74-dependent inflammatory signaling between RPE and infiltrating immune cells. Histidine supplementation or AKT2 phospho-state modulation attenuated systemic immune activation and rescued retinal degeneration. These findings identify histidine-axis dysregulation as a mechanistic bridge between diet-induced microbiome changes, metabolic stress, immune aging, and retinal degeneration. - Source: PubMed
Publication date: 2026/04/17
Ghosh SayanKoontz VictoriaXin YingBammidi SridharMeyer DominiqueWang HaochenBabu Vishnu SureshDutta PujaCherukaraveedu DurgadasMohanakrishnan Shreevadsaa AMondal Anupam KDas JagannathNguyen JennySoundararajan AvinashAdekale Idris ABhaumik DulalHose StaceyRowan SheldonPattabiraman Padmanabhan PKannan Rangaramanujam MHanda James TYi JiSripathi Srinivasa RQian JiangSinha Debasish - Osteoarthritis (OA) represents the most common degenerative joint disease, with emerging evidence linking it to lysosomal dysfunction and ferroptotic cell death. This study aimed to identify candidate biomarkers associated with lysosomal function and ferroptosis in OA, thereby providing a theoretical basis for subsequent experimental research. - Source: PubMed
Publication date: 2026/04/21
Fan YuFan FurongXie JunhaoChen GuoliangXu JingzheYang Chengbin