SLC7A5 Antibody
- Known as:
- SLC7A5 Antibody
- Catalog number:
- 48-216
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC7A5 Antibody
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
- Naive B cells exit quiescence and enter a proliferative state upon activation, ultimately differentiating into antibody-secreting or memory B cells. Toll-like receptor (TLR) ligands, such as lipopolysaccharide (LPS), can serve as physiological stimuli to initiate this transition. Using quantitative proteomics, we show that TLR4 engagement induces metabolic reprogramming in murine B cells, increasing the expression of amino acid transporters and cholesterol biosynthetic enzymes. The amino acid transporter SLC7A5 is markedly upregulated following LPS stimulation, and conditional deletion of impairs B cell proliferation, underscoring its essential role in B cell activation. LPS also elevates intracellular cholesterol levels, and inhibition of the rate-limiting enzyme HMG-CoA reductase blocks proliferation. This effect was mediated by a dual requirement for cholesterol metabolism and protein prenylation downstream of HMG-CoA reductase. Notably, this was not unique to TLR4 signalling but is also observed in B cells activated via TLR7, TLR9, CD40, or the B cell receptor. Together, these findings reveal that metabolic rewiring, including amino acid uptake and cholesterol metabolism, is an essential feature of B cell activation and proliferation. - Source: PubMed
Publication date: 2026/05/21
Cheung Dana M SRazsolkov MomchilBonacina FabriziaAndrews StephenSumoreeah Megan CSinclair Linda VHowden Andrew J MArthur J Simon C - The adult mammalian intestinal epithelium is constantly self-renewed via cell proliferation in the crypt. Earlier studies have revealed many genes and pathways important for regulating intestinal epithelial cell proliferation and differentiation to maintain adult epithelial homeostasis. Of interest among them is system L amino acid transporter 1 (), also known as slc7a5. Slc7a5 can transport thyroid hormone and large, neutral amino acids such as leucine and tryptophan. It can activate mTORC1 to increase cell proliferation by transporting amino acid. We have previously shown that slc7a5 is highly expressed in adult mouse intestinal crypt and that intestinal epithelial cell-specific knockout () of slc7a5 ( ) reduces mTORC1 signaling. Unexpectedly, intestinal crypts have increased cell proliferation in the small intestine. There is also a drastic reduction in mature Paneth cells, suggesting a possible indirect effect of slc7a5 on cell proliferation by regulating secretory cell differentiation. Here, we have generated a tamoxifen-inducible intestinal epithelial-specific slc7a5 knockout line (slc7a5 ). We show that inducible knockout of slc7a5 in adult mice also leads to reduced mature Paneth cells and increased cell proliferation in the crypt, revealing that slc7a5 is important for adult intestinal epithelial homeostasis. Kinetically, the reduction of mature Paneth cells occurs before the increase in cell proliferation. Furthermore, in stable intestinal epithelial cell-specific knockout ( ) animals, a reduction in mature Paneth cells occurs soon after mature Paneth cells are first formed during post-natal development while an increase in crypt cell proliferation occurs later by postnatal day 28 after intestinal maturation is complete. These findings support a mechanism where slc7a5 affects cell proliferation indirectly by regulating Paneth cell differentiation to maintain adult intestinal epithelial homeostasis. - Source: PubMed
Publication date: 2026/04/16
Bao LingyuPeng ZhaoyiShi BingyinShi Yun-Bo - 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