Ask about this productRelated genes to: SLC38A1 Blocking Peptide
- Gene:
- SLC38A1 NIH gene
- Name:
- solute carrier family 38 member 1
- Previous symbol:
- -
- Synonyms:
- ATA1, NAT2, SAT1
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-22
- Date modifiied:
- 2015-12-08
Related products to: SLC38A1 Blocking Peptide
Related articles to: SLC38A1 Blocking Peptide
- : Tumor cells can reprogram their metabolism, constituting a hallmark of cancer that plays a crucial role in tumor progression. As tumor cells exhibit an increased demand for nutrients, e.g., amino acids, they rely on extracellular sources and show deregulation of transport proteins. Among these, SNAT1 (SLC38A1) is described as the loader for glutamine that is responsible for the main influx of this amino acid. The aim of this study was to assess the molecular function of SNAT1 in melanoma regarding its role in amino acid transport and regulation of cellular metabolism. : siPool-mediated downregulation of SNAT1 expression in melanoma cell lines was used to investigate the molecular function of this protein. Glutamine transport was assessed by measuring the intracellular and extracellular concentrations of glutamine. Regulation of downstream effectors was evaluated with qRT-PCR and Western Blot. Metabolism was investigated by performing Seahorse flux analysis. Mitochondrial staining was examined via flow cytometry. Protein interaction was assessed with Co-IP, and in silico modeling of protein interaction was performed with AlphaFold3. : In this study, we uncovered the new finding that SNAT1 is not primarily implicated in glutamine influx into melanoma cells but in signaling in response to extracellular glutamine. We identified P62 and cMYC as downstream effectors of SNAT1. By activating the P62/cMYC-axis and target genes of cMYC, SNAT1 modulates the metabolism of melanoma cells depending on the glutamine level. SNAT1 and P62 are interaction partners. : This finding newly suggests that SNAT1 may function as a sensor or receptor ("transceptor") for glutamine rather than being a direct and primary glutamine transporter, and could open up new therapeutic options targeting melanoma cells. - Source: PubMed
Publication date: 2026/03/25
Lörentz SandraBöhme-Schäfer InesKönig JörgSticht HeinrichBosserhoff Anja Katrin - Primary biliary cholangitis (PBC) is a chronic autoimmune liver disease that causes bile duct damage, liver fibrosis, and cirrhosis, significantly affecting patients' lives and healthcare costs. Early diagnosis is critical but is hindered by the limited sensitivity of existing biomarkers, particularly in patients who are negative for anti-mitochondrial antibodies. This limitation underscores the need for more reliable biomarkers. Our study focuses on secretory proteins as potential diagnostic biomarkers and aims to elucidate gene expression profiles associated with PBC using bioinformatics methods and machine learning. We identified 827 downregulated and 639 upregulated genes related to mitochondrial function and immune pathways. Additionally, Weighted Gene Co-expression Network Analysis revealed a blue module comprising 1,949 genes linked to PBC. Machine learning identified between 14 and 18 key diagnostic genes. Using a Gaussian Mixture Model, we achieved an area under the curve of 0.96, indicating excellent diagnostic performance. Notable genes included the upregulated CSF1R, PLCH2, and SLC38A1, as well as the downregulated CST7. Animal experiments further supported these bioinformatics findings. Our research highlights secretory proteins as promising biomarkers for the early diagnosis of PBC, with potential applications in developing precise diagnostic tools and personalized therapies. This work paves the way for future studies involving larger cohorts and multi-omics data. - Source: PubMed
Publication date: 2025/12/30
Xu ZihaoCai YueLiu YifanXu JunGuo ShengZhou LihanJi YangZhan LeiCheng Liangbin - Amino acid (AA) uptake is essential for T cell metabolism and function, but how tissue sites and inflammation affect CD4 T cell subset requirements for specific AAs remains uncertain. Here, we tested CD4 T cell AA demands with in vitro and in vivo CRISPR screens and identified subset- and tissue-specific dependencies on the AA transporter SLC38A1 (SNAT1). While dispensable for T cell persistence and expansion in vivo in lung inflammation, SLC38A1 was critical for Th1, but not Th17, cell-driven experimental autoimmune encephalomyelitis (EAE) and contributed to Th1 cell-driven inflammatory bowel disease. SLC38A1 deficiency reduced mTORC1 signaling and glycolytic activity in Th1 cells, in part by reducing glutamine uptake and disrupting hexosamine biosynthesis and redox regulation. Pharmacological inhibition of SLC38 transporters also delayed Th1-mediated EAE but did not affect lung inflammation. CD4 T cells thus have subset- and tissue-specific nutrient transporter dependencies that may guide new metabolic approaches for selective immunotherapies. - Source: PubMed
Publication date: 2026/03/23
Sugiura AyakaBeier Katherine LChi ChanningHeintzman Darren RYe XiangWolf Melissa MPatterson Andrew RCephus Jacqueline-YvonneHong Hanna SPerera Jeffrey MLyssiotis Costas ANewcomb Dawn CRathmell Jeffrey C - Solute carrier family 38 member 1 (SLC38A1) is a principal glutamine transporter associated with solid tumor development and progression. However, it has rarely been investigated in hematologic malignancies. This study aimed to assess the expression status and correlation of SLC38A1 with clinicopathological features in acute leukemia patients. In this cross-sectional study, SLC38A1 expression was evaluated via RTQ-PCR in 140 denovo acute leukemia patients (70 adult AML cases and 70 pediatrics B-ALL cases) and 70 healthy controls (40 adults and 30 children for the AML and B-ALL groups, respectively). Statistical analysis was done by IBM SPSS software version 20. Other clinical and laboratory data including genetic testing, when available, were extracted from the Hospital Information System (HIS). We found that SLC38A1 was overexpressed in both types of acute leukemia patients compared with controls (Median (IQR): 4.26(11.32) for AML vs. 1.08(1.68) for control; = 0.026, and 5.76(15.97) for B-ALL vs. 0.65(1.18) for control; = 0.019). The distribution of FAB and WHO classifications varied significantly between AML patients with high SLC38A1 expression compared to those with low expression ( = 0.005 and = 0.017, respectively). In addition, B-ALL patients in low or high SCL38A1 expression groups showed various distributions regarding WHO classification ( = 0.03). In Kaplan-Meier analysis, both AML and B-ALL patients with SLC38A1 had shorter overall survival (OS) compared to SLC38A1 patients ( < 0.001 and = 0.007, respectively). Multivariate analysis confirmed that SLC38A1 upregulation was an independent indicator for prognosis in acute leukemia patients (HR = 3.856, 95% CI = 1.766-8.421, = 0.001 for AML and HR = 2.718, 95% CI = 1.086-6.797, = 0.03 for B-ALL). Our results indicated that overexpression of SLC38A1 was correlated with poor OS in both AML and B-ALL patients. Therefore, SLC38A1 may be used as a prognostic marker in acute leukemias. - Source: PubMed
Publication date: 2025/05/10
Khajavi MaryamAyatollahi HosseinKeramati Mohammad RezaMazhari ArefehSheikhi MaryamEsmaily HabibollahSadeghian Mohammad HadiMehrad-Majd HassanBoroumand-Noughabi Samaneh - Prior research has indicated that membrane transporter proteins may play a role in tumorigenesis, progression, and mechanisms of drug resistance in hepatocellular carcinoma (HCC) by affecting the transport of drugs, nutrients, and metabolites. Therefore, a comprehensive elucidation of the role of membrane transporter protein-related genes (MTPRGs) in the outcome of those suffering with HCC is essential. - Source: PubMed
Publication date: 2026/02/12
Xiao YifuZhang GuoqingZhao Hui