Ask about this productRelated genes to: SLC7A14 antibody
- Gene:
- SLC7A14 NIH gene
- Name:
- solute carrier family 7 member 14
- Previous symbol:
- -
- Synonyms:
- KIAA1613, PPP1R142
- Chromosome:
- 3q26.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-06
- Date modifiied:
- 2015-12-08
Related products to: SLC7A14 antibody
Related articles to: SLC7A14 antibody
- Solute carrier (SLC) family genes govern transmembrane transport and cellular metabolism, yet their systematic roles from Helicobacter pylori infection to gastric cancer (GC) remain undefined. By integrating multiple GEO datasets with weighted gene co-expression network analysis, differential expression, and machine learning algorithms, we identified seven core SLC genes (SLC9A9, SLC43A2, SLC16A6, SLC7A14, SLC28A3, SLC4A11, SLC5A2) for H. pylori infection and nine (SLC1A3, SLC2A3, SLC15A3, SLC19A3, SLC2A12, SLC16A4, SLC25A4, SLC9A7, SLC28A3) for GC. Logistic regression models achieved high diagnostic accuracy (AUC = 0.976 and 0.874, respectively). Immune infiltration analysis revealed distinct correlation patterns: SLC4A11 and SLC5A2 associated with activated mast cells, neutrophils, and M2 macrophages in infection, while SLC1A3 and SLC2A3 correlated broadly with M1/M2 macrophages and activated CD4 T cells in GC. Enrichment analyses confirmed involvement in transmembrane transport, immune-related pathways, and cancer signaling. Transcription factor prediction identified CEBPB, RELB, and STAT5A as key upstream regulators. Molecular docking demonstrated strong binding affinities between SLC proteins and repurposable compounds (3'-azido-3'-deoxythymidine, CHEMBL1182312, quinine). This study provides the first systematic characterization of SLC family expression across the H. pylori-GC continuum, identifying potential diagnostic biomarkers and therapeutic targets that warrant further experimental validation. - Source: PubMed
Publication date: 2026/07/25
Lv NuonanHe XueCai TingXu YingtingXie JieZhao XuelinYang BinfangLiu XuemeiZhang Minglin - Cationic amino acid transporters (CATs), encoded by the SLC7A family, play essential roles in the uptake of arginine and other cationic amino acids, thereby regulating cellular metabolism, signaling, and immune responses. Among SLC7A transporters, SLC7A1-4 constitute the classical CAT family and have emerged as important regulators of tumor biology. Arginine is increasingly recognized as a critical metabolic resource within the tumor microenvironment. Consequently, dysregulated CAT expression can affect both cancer cell fitness and tumor-immune interactions. In this review, we summarize current knowledge regarding the biological and pathological roles of SLC7A1-4 in cancer. SLC7A1 is broadly associated with enhanced tumor growth, metabolic adaptation, and therapeutic resistance through increased arginine uptake. In contrast, SLC7A2 exhibits context-dependent functions, displaying both tumor-promoting and tumor-suppressive activities depending on tumor type and immune context regulation. Emerging evidence also implicates SLC7A3 in metastatic progression through transcriptional programs that increase arginine availability, whereas the physiological role of SLC7A4 remains largely unresolved. Despite its structural similarity to other CAT family members, convincing evidence for its membrane localization, cationic amino acid transport activity, and cancer-associated functions is still lacking. We further discuss the mechanistic pathways linking CAT to cancer progression and tumor-immune metabolic competition. Finally, we highlight key unresolved questions, including functional redundancy among CAT family members, context-dependent biological effects, and the uncertain role of SLC7A4. A deeper understanding of CAT biology may provide new opportunities for therapeutic strategies targeting amino acid metabolism in cancer. - Source: PubMed
Publication date: 2026/07/12
Myo Oo Thant ThantSaito Yasuhiro - SLC7A14 is a putative amino acid transporter whose physiological role remains poorly characterized, despite its association with retinal degeneration, auditory defects, and metabolic dysfunctions. Confocal microscopy was performed in HEK293 transiently transfected with the human SLC7A14 (hSLC7A14), demonstrating a lysosomal localization, as previously suggested. To carry on functional and kinetic characterization, the protein was overexpressed in E. coli, and purified from insoluble fraction through affinity chromatography followed by SEC with a yield of 156 mg/L of bacterial cell culture. The homogeneous hSLC7A14 showed an apparent molecular mass of 72 kDa on SDS-PAGE and was reconstituted into proteoliposomes for functional assays. hSLC7A14 showed high specificity towards arginine, not histidine or glutamine, with a measured Km of 1.2 ± 0.21 mM. The arginine transport was inhibited by cysteine and threonine, but not by other amino acids or GABA. Inhibition kinetics identified metformin as an inhibitor of the transporter showing a mixed type of inhibition with a measured Ki in the same order of that of arginine. These findings are in agreement with hSLC7A14 being a specific lysosomal arginine transporter, with potential involvement in the mTORC1 signalling. The described results represent a first step to further elucidate hSLC7A14 role in human physiology and disease. Moreover, the identification of experimental conditions for measuring specific transport activity will allow screening of ligands as inhibitors or functional modulators opening perspectives for structure/function relationship studies. - Source: PubMed
Publication date: 2026/06/26
Giudice DeborahBarone FrancescaMazza TizianoScalise MariafrancescaConsole LaraIndiveri Cesare - Fatigue is a common but poorly understood issue in type 2 diabetes (T2DM) that affects quality of life. Although ceRNA networks regulate disease progression, their role in T2DM-related fatigue (F-T2DM) is unclear. This study developed a circRNA-mediated ceRNA network to uncover the molecular interactions causing fatigue in F-T2DM. The study included healthy control group (Control, n = 21), F-T2DM group (n = 21), and non-fatigue type 2 diabetes patients (NF-T2DM, n = 21). By combining high-throughput sequencing to screen differentially expressed circRNAs (F-T2DM vs Control: 1144; F-T2DM vs NF-T2DM: 1303) and mRNAs (F-T2DM vs Control: 912; F-T2DM vs NF-T2DM: 1190), it was found that hsa_circ_0078539 and hsa_circ_0026239 were significantly upregulated in F-T2DM compared to both Control and NF-T2DM groups, and their host genes were involved in cytoskeleton remodeling. The GO/KEGG enrichment analysis combined with weighted gene co-expression network (WGCNA) of F-T2DM compared with Control indicated that the core pathways of F-T2DM focused on actin cytoskeleton dynamic regulation, AMPK signaling pathway, tricarboxylic acid cycle, and oxidative stress response. In the enrichment analysis of F-T2DM and NF-T2DM, cytoskeleton dynamics regulation, AMPK signaling pathway, and tricarboxylic acid cycle were further enriched, and the specific activation of reactive oxygen metabolism balance and AGE-RAGE pathway was also observed. Further, through multi-database prediction and experimental verification, a F-T2DM-specific ceRNA network was constructed, and key regulatory axes hsa_circ_0044623/hsa-mir-129-5p/MYLK3, hsa_circ_0002622/hsa-mir-200b-3p/RAB21, and hsa_circ_0078539/hsa-mir-4695-3p/SLC7A14 were screened out. The ceRNA regulatory network in human and animal samples was confirmed using RT-qPCR. These axes drive the pathological process by regulating myocardial contractility efficiency, glucose transport, mitochondrial energy metabolism, and insulin signaling pathway. This study clarified the molecular regulatory mode of patients with fatigue type 2 diabetes from the perspective of ceRNA network, providing a new direction for the research on diabetes classification and diagnosis. - Source: PubMed
Publication date: 2025/09/02
Zhen Xian-JieWu TaoZhang MinZhang Chu-YueLiu Rui-JieJiang JingJiang Guang-Jian - Benign Metastasizing Leiomyoma (BML) and Intravenous Leiomyomatosis (IVL) are rare uterine-derived smooth muscle tumors. Although both exhibit histologically benign and similar features, they demonstrate aggressive biological behaviors. Currently, molecular genetic studies on BML and IVL are limited, and no comparative research on their genetic variations has been reported. To investigate the genetic basis underlying their shared aggressive phenotypes, this study employs whole-exome sequencing (WES) to conduct a molecular genetic comparison between the two entities. The aim is to explore potential genetic variations that may reveal common pathological pathways shared by these diseases, thereby enhancing our understanding of the molecular mechanisms driving their invasiveness. - Source: PubMed
Publication date: 2025/05/28
Li JinZeng JiafeiLuo ShuaiWang Jinjing