SLC7A5 antibody
- Known as:
- SLC7A5 (anti-)
- Catalog number:
- orb77270
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- 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
- 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 - Gastrointestinal (GI) cancers remain a leading cause of cancer-related mortality worldwide, underscoring the urgent need for reliable, non-invasive diagnostic biomarkers. Circular RNAs (circRNAs), characterized by high stability and tissue specificity, have emerged as promising molecular indicators for early cancer detection. This study aimed to evaluate the diagnostic accuracy of circular RNAs (circRNAs) for detecting gastrointestinal (GI) cancers, including gastric cancer (GC), hepatocellular carcinoma (HCC), esophageal cancer (EC), colorectal cancer (CRC), and pancreatic cancer (PC). - Source: PubMed
Publication date: 2025/12/18
Bahramirad JilaMoradi YousefMoradi GhobadDehghanbanadaki HojatAbdi MohammadNasseri Sherko - B cells are an essential component of humoral immunity, and B cell depletion therapies have clinically succeeded in eliminating cancerous B cells and treating autoimmune diseases. Here, we report an immune-independent function of B cells that spatially and metabolically drives exercise capacity. During exercise, B cell deficiency reduces transforming growth factor (TGF)-β1 production, which alters hepatic glutamate metabolism and decreases blood and muscle glutamate. Mechanistically, B cell-derived TGF-β1 transcriptionally upregulates hepatic glutaminase 2 (GLS2) and solute carrier family 7 member 5 (SLC7A5) expression, increasing glutamine catabolism and thus glutamate production in the liver. The resulting increase in glutamate fosters skeletal muscle calcium oscillations, calmodulin-dependent protein kinase (CaMK) kinase activity, and mitochondrial biogenesis, thereby improving exercise performance. Thus, we identify a metabolite-driven liver-muscle connection that regulates exercise capacity, linking B cell function to skeletal muscle calcium signaling via alteration of hepatic glutamate metabolism. - Source: PubMed
Publication date: 2026/04/17
Mao YouxiangXia ZiyanPan XuXia WenjunJiang Peng