Ask about this productRelated genes to: SLC7A1 antibody
- Gene:
- SLC7A1 NIH gene
- Name:
- solute carrier family 7 member 1
- Previous symbol:
- ERR, ATRC1
- Synonyms:
- CAT-1, HCAT1, REC1L
- Chromosome:
- 13q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-02-17
Related products to: SLC7A1 antibody
Related articles to: SLC7A1 antibody
- circRNA is known to have regulatory functions across different cancers. Nevertheless, its regulatory functions in non-small cell lung cancer (NSCLC) are unknown. The present investigation aimed to research circ-FSCN1 expression in NSCLC cells and tissues employing high-throughput sequencing (HTS). NSCLC cells were investigated utilizing the CCK-8, EdU, and Transwell assays. Luciferase reporter assays were employed to verify circ-FSCN1 and its downstream target. Tumorigenesis and metastasis assays were performed to detect the role of circ-FSCN1 in NSCLC. Immunofluorescence was used to detect ROS deposition. The data indicated that the expression of hsa_circ_0004175 (circ-FSCN1) was elevated in NSCLC tissues and cells. The downregulation of circ-FSCN1 inhibited cellular migration and proliferation in the experiments. miR-506-3p downregulation or SLC7A1 overexpression reversed the suppression effects of sh-circ-FSCN1 on the proliferation and migration ability of H1299 and A549 cells. SLC7A1 overexpression reversed the inhibitory effects of miR-506-3p on the proliferation and migration ability of H1299 and A549 cells. The current investigation revealed that inhibiting miR-506-3p or overexpressing SLC7A1 reversed the enhancing effects of sh-circ-FSCN1 on ROS accumulation in H1299 and A549 cells. SLC7A1 overexpression reversed the enhancing effects of miR-506-3p on ROS accumulation in A549 and H1299 cells. Our investigation discovered that circ-FSCN1 affects ferroptosis and cell viability via the miR-506-3p/SLC7A1 pathway in NSCLC. circ-FSCN1 can function as a potential NSCLC diagnostic biomarker and therapy target. - Source: PubMed
Publication date: 2026/05/09
Yu WenxiLiu JiaoJin MingmingHuang GangHuang Qingqing - The greyhound has been strongly selected for competitive racing. Here, we present the first comprehensive population genomic analysis of racing greyhounds (n = 54) in the context of 14 other dog breeds (n = 352) using 473K single nucleotide polymorphism (SNP) genotypes. Inbreeding in the greyhound (FROH = 0.47) was higher than in most other breeds, reflecting positive selection for athletic traits but also raising concerns about potential health impacts. Although very long runs of homozygosity (ROH) were less common in the greyhound than in some breeds, large ROH islands suggest that selection for advantageous traits is relatively recent. Genomic regions under strong selection overlapped with ROH islands on CFA2, CFA4, CFA9, CFA10, CFA25 and CFA28 and contained candidate genes with marked allele frequency differences relative to other breeds. Notably, the strongest selection signal overlapped with the longest ROH island, encompassing the SLC46A3, POLR1D, FLT3, SLC7A1, MTUS2, LHFPL6, USPL1 and USP12 genes that have biological functions in vision, craniofacial morphology, neurological adaptability and skeletal, cardiac and muscle biology, implicating them in shaping the greyhound's morphological and athletic phenotype. These results provide insights into the selection pressures in the racing greyhound, identifying key genomic regions and candidate genes that may underlie racing capabilities, and importantly for animal welfare, provide a framework for managing inbreeding to optimize health and performance for future generations. - Source: PubMed
Han HaigeBlackett Tiffany ACampbell Madeleine L HHoltby Amy RebeccaMcGivney Beatrice AHill Emmeline Wynne - Human solid tumors such as hepatocellular carcinomas (HCC) establish a complex immunosuppressive tumor microenvironment (TME) that undermines the efficacy of existing immunotherapies such as chimeric antigen receptor T (CAR T) cell therapy. To advance immunotherapy for HCC, it is crucial to delineate the molecular mechanisms that drive TME formation and immune evasion. - Source: PubMed
Publication date: 2026/04/09
Zhu LishengWu MengFeng BingbingZhang YuXu YangYu Lili - At the blood-tissue interface, vasculature luminal surface is critical for molecular transport, signaling transduction, and cell extravasation. Here, we present a method for proteomic profiling of the vasculature luminal surface in vivo, broadly applicable to any vertebrate. Quantitative mass spectrometry revealed the luminal surface proteome of the mouse brain vasculature and its temporal evolution from development to aging. In vivo genetic perturbation found that the arginine transporter SLC7A1 and the nitric oxide synthase NOS3 are needed for blood-brain barrier integrity in neonatal but not adult mice, whereas the hyaluronan degradation enzyme HYAL2 safeguards the barrier throughout the lifespan. By characterizing the proteomic dynamics of the vasculature luminal surface, the study links the metabolism of nitric oxide and hyaluronan to blood-brain barrier integrity. - Source: PubMed
Publication date: 2026/04/09
Zhu ZijianJiang ZuzhiWang YupuNguyen KhanhZhang YuxiangLian Cameron GenxuanMani D RZheng JunDing LangGao Shihong MaxXia Ruyue AlpsKuszpit AnneLindo SarahLopez CrystallLindsey CatherineGroff BrookeChen XinhongWu JiahuiXia WeiliangLi WeiLiu XiaorongGradinaru VivianaCarr Steven AUdeshi Namrata DLi Jiefu - Mutations in several translation initiation factors are closely associated with premature ovarian insufficiency (POI). In this study, we demonstrated that the conditional knockout of eukaryotic initiation factor 2 (eIF2) subunits Eif2s1 and Eif2s2 in mouse oocytes caused oocyte apoptosis within the early growing follicles. Subsequent research indicated that the depletion of Eif2s2 in oocytes reduced the levels of mitochondrial fission-related proteins (p-DRP1, FIS1 and MFF) and increased the mRNA and protein levels of the integrated stress response (ISR)-related factors (ASNS, SLC7A1, GRB10 and PSAT1). Consistent with this, the depletion of Eif2s2 in oocytes resulted in mitochondrial dysfunction characterized by elongated form, aggregated distribution beneath the oocyte membrane, decreased mitochondrial membrane potential and ATP content, and excessive accumulation of reactive oxygen species (ROS). At the same time, the depletion of Eif2s2 in oocytes led to increased levels of DNA damage response proteins (γH2AX, p-CHK2 and p53) and proapoptotic proteins (BAX and PARP1), as well as decreased the levels of anti-apoptotic protein BCL-xL. Collectively, these findings indicate that the depletion of eIF2 subunits in mouse oocytes leads to oocyte apoptosis within the early growing follicles, attributed to the impaired translation of mitochondrial dynamics regulatory proteins and then the upregulated ROS levels and DNA damage. This study provides new insights into pathogenesis and genetic diagnosis for POI. - Source: PubMed
Publication date: 2026/02/02
Liu HuiyuWang WeiyongLi BiaoLiu ShuangWei HongweiZhou WenjunHao TiantianWei YingZhang XiaodanZhang Meijia