Rat Anti-Mouse CD98, FITC-labeled
- Known as:
- Rat Antibody toMouse CD98, fluorecein-labeled
- Catalog number:
- 129-10179
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD98 FITC-labeled
Related genes to: Rat Anti-Mouse CD98, FITC-labeled
- Gene:
- SLC3A2 NIH gene
- Name:
- solute carrier family 3 member 2
- Previous symbol:
- MDU1
- Synonyms:
- 4T2HC, 4F2, NACAE, CD98, CD98HC, 4F2HC
- Chromosome:
- 11q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-15
- Date modifiied:
- 2016-02-17
- 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: Rat Anti-Mouse CD98, FITC-labeled
Related articles to: Rat Anti-Mouse CD98, FITC-labeled
- 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 - Colorectal cancer (CRC) is the second leading cause of cancer-related deaths worldwide, with up to 20% of patients presenting with metastatic disease at diagnosis. The clinical relevance of amino acid transporters ASCT2 and LAT1 in CRC, particularly Caucasian populations, remains underexplored. This study evaluates the prognostic impact of single nucleotide polymorphisms (SNPs) in the genes encoding these transporters (, and ) in a European population. - Source: PubMed
Lopes CatarinaMacedo-Silva CatarinaFarinha MónicaCosta JoãoPinelas SofiaVilas-Boas IsabelDinis-Ribeiro MárioPereira CarinaMedeiros Rui - The hyperactivation of the transcriptional coactivator YAP, a downstream effector of the Hippo pathway, has been implicated in the initiation and progression of human cancers including glioblastoma (GBM), but the underlying mechanisms remain elusive. In this study, we demonstrate that methionine promotes YAP activation through PRMT5-mediated symmetrical dimethylation (sDMA) at a conserved arginine residue within five conserved LATS-targeting motifs (HXRXXS), with R124 identified as the primary site of modification. R124 sDMA (R124me2s) serves as a physiological protective mechanism against LATS-mediated inhibitory phosphorylation of YAP at Ser127, thereby facilitating YAP nuclear translocation and enhancing its transcriptional activity. Moreover, YAP R124 sDMA drives tumor methionine addiction and tumorigenicity of GBM through a feedforward loop in which YAP transcriptionally upregulates PRMT5 and the methionine transporters SLC3A2/SLC7A5. Furthermore, radiation activates PRMT5-YAP-SLC3A2/7A5 axis to promote GBM cell survival. Inhibiting this signaling axis in combination with radiotherapy impairs intracranial xenograft growth, resulting in significant survival extensions for treated animals. Overall, our findings uncover a previously unrecognized regulatory axis where PRMT5-mediated R124me2s governs YAP activation through a feedback mechanism, presenting novel therapeutic vulnerabilities in GBM. - Source: PubMed
Publication date: 2026/02/07
Luo MeiWu ShiyuHuang ChenxinZheng ZiyuanXia QiaoxiLi YonghuaZhou XiaoHong ShihongZhong RonghuiLi WeijieWang BotaoCheng Shi-YuanJiang XiaobingLi JunjunHuang Tianzhi - Alzheimer's disease (AD) is a common neurodegenerative disorder; however, its molecular complexity remains poorly understood. Single-cell analysis can reveal the molecular changes in AD in different types of brain cells. In this study, we integrated single-cell sequencing and transcriptome data to explore the molecular mechanism of integrated stress response (ISR) in AD. Analysis of the GSE264648 (49 cases) and GSE48350 (253 cases) datasets showed that the integrated stress response (ISR) activity of endothelial cells in patients with AD was significantly increased compared with normal control group. Six key genes (BTG1, EPB41L4A, HERPUD1, SLC3A2, SLC7A11, and SLC7A5) were screened by combining the Least Absolute Shrinkage and Selection Operator (LASSO) regression and the random forest algorithm. Urine test for β-amyloid protein, Clinical Dementia Rating, modified Hachinski Ischemia Scale, Hamilton Depression Scale, Hamilton Anxiety Scale and head magnetic resonance imaging were used to screen cilinical subjects, and then verified the six key genes in their blood samples. These key genes are enriched in inflammatory pathways such as NF-κB and TNF, and are closely related to immune cell infiltration (e.g., M2 macrophages and neutrophils). This research also revealed the association between key and core genes of AD (e.g., APOE) and their clinical predictive value, providing new clues for mechanistic research and targeted therapy of AD. - Source: PubMed
Publication date: 2026/01/06
Sheng NingWang Hong-YanSong KunZheng YongZong Zi-YingGe Jin-WenWu Da-HuaWang Ya-Han - The rewiring of amino acid (AA) metabolism is a key characteristic of cancer metabolism. Cells can only synthesize nonessential AAs, but if the demands of highly proliferating cells don't meet the endogenous synthesis capacity, AAs must be acquired from outside. SLC7 belongs to the solute carrier transporters (SLC) superfamily and acts as a passive facilitative or secondary AA active transporter. LAT1/SLC7A5 acts as an antiporter that mediates the influx of several AAs into cells in exchange for the efflux of intracellular substrates. In tumor cells, LAT1/SLC7A5 overexpression is closely associated with proliferation, invasion, metastasis, and poor clinical prognosis. Formyl peptide receptor 2 (FPR2) belongs to the FPR family of GPCRs. Its activation regulates several biological processes and triggers NADPH oxidase assembly and, consequently, reactive oxygen species (ROS) generation. FPR2 stimulation also induces an increase in SLC1A5/ASCT2 and SLC7A11/xCT expression, which correlates with enhanced glutamine and cystine uptake, respectively. Herein, we analyze the LAT1/SLC7A5-mediated uptake of several essential AAs in FPR2-stimulated CaLu-6 and HCC1937 cells and prove: (i) the redox regulation of both LAT1/SLC7A5 and 4F2hc/SLC3A2/CD98, which form a heterodimer on the plasma membrane; (ii) the redox activation of the mTOR pathway and, in turn, of S6K1 and 4E-BP1, which stimulate protein synthesis; (iii) c-Myc and miR-126 regulation, which control LAT1/SLC7A5 synthesis at the transcriptional and post-transcriptional level, respectively. These findings provide new approaches for the development of novel therapeutic strategies for the treatment of human cancers. - Source: PubMed
Publication date: 2025/12/21
Cassese MyrhiamBrignola ChiaraMarrone StefanoEsposito GabriellaAmmendola RosarioCattaneo Fabio