SLC39A7 antibody (FITC)
- Known as:
- SLC39A7 (anti-) (fluorecein)
- Catalog number:
- orb9811
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SLC39A7 antibody (FITC)
Related genes to: SLC39A7 antibody (FITC)
- Gene:
- SLC39A7 NIH gene
- Name:
- solute carrier family 39 member 7
- Previous symbol:
- HKE4
- Synonyms:
- H2-KE4, D6S2244E, KE4, RING5, ZIP7
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-25
- Date modifiied:
- 2016-10-05
Related products to: SLC39A7 antibody (FITC)
Related articles to: SLC39A7 antibody (FITC)
- Zinc homeostasis regulated by ZIP transporters is critical for tumor glycolytic reprogramming and progression, yet the role of specific ZIP family members in lung adenocarcinoma (LUAD) remains unclear. This study aimed to identify the key ZIP transporter in LUAD and elucidate its molecular mechanisms and therapeutic value. siRNA-based functional screening of the ZIP family was performed in A549 and PC9 cells. A combination of in vitro cellular assays, in vivo animal models, clinical sample analysis and bioinformatics was used to validate the function of ZIP7 and explore its regulatory mechanisms. ZIP7 (SLC39A7) was identified as a critical driver of glycolysis and proliferation in LUAD. It was significantly upregulated in LUAD tissues and cell lines. Mechanistically, ZIP7 increased inhibitory phosphorylation of GSK3β at Ser9 to stabilize NRF2, maintained low intracellular ROS levels, and sustained mTOR signaling to promote glycolytic flux. ZIP7-induced lactate secretion also drove M2-like macrophage polarization and PD-L1 upregulation to establish an immunosuppressive microenvironment. Notably, genetic or pharmacological inhibition of ZIP7 markedly enhanced the antitumor efficacy of anti-PD-1 therapy in vivo. ZIP7 is a pivotal oncogenic zinc transporter in LUAD that drives tumor progression via metabolic reprogramming and immune remodeling. Targeting ZIP7 represents a promising strategy to improve the efficacy of anti-PD-1 immunotherapy for LUAD. - Source: PubMed
Publication date: 2026/06/01
Tang ZhihuaShi YueliJiang XinyuanJiang SujingMaihemuti NuerailiZhang JieTang BufuXu Zhiyong - : ASD is a class of neurodevelopmental disorders with onset in early childhood, whereas AD is a common chronic inflammatory skin disease. An increasing number of studies suggest that immune dysregulation and inflammatory responses play important roles in the onset and progression of both conditions; however, their shared molecular mechanisms remain unclear. : First, ASD-related and AD-related datasets were obtained from the GEO database. After removal of batch effects, the common DEGs between the two diseases were identified. Subsequently, 107 machine learning-based model configurations were employed to screen for key genes. Functional enrichment analyses and PPI network construction were performed to systematically explore their potential functions. Finally, the CIBERSORT was applied to analyze immune cell infiltration and to assess the correlation between hub gene expression and immune cell infiltration. : 164 common genes between ASD and AD were identified. GO and KEGG enrichment analyses revealed that these shared differentially expressed genes were mainly enriched in pathways related to immune regulation and inflammatory responses, suggesting that immuno-inflammatory processes may constitute an important biological basis linking ASD and AD. Further screening and validation using machine learning identified , , , , , , and as hub genes serving as common potential biomarkers for both diseases. Among them, , , and may represent key shared genes and demonstrated good diagnostic value in ROC curve and nomogram analyses. In addition, immune infiltration analysis indicated that these key genes were significantly correlated with the infiltration levels of multiple immune cell types, further supporting their potential roles in immune regulation. : This study reveals potential shared immuno-inflammatory molecular mechanisms between ASD and AD. Genes screened based on 107 machine learning models were verified as potential diagnostic biomarkers for both diseases after integrated analysis, providing a theoretical basis for further investigation of their immune-related pathogenesis and early clinical diagnosis. - Source: PubMed
Publication date: 2026/05/12
Yang RuilingZhang FushenHuang Jufang - Zinc homeostasis is crucial for various biological processes, including gene regulation, signal transduction, and proteostasis. ZIP7 is a membrane transporter that exports zinc ions (Zn) from the lumen of the endoplasmic reticulum (ER) to the cytosol, and its dysfunction causes ER stress, although the underlying mechanism remains unclear. Here, we show that ZIP7 inhibition increases the labile Zn concentration in the ER to micromolar levels, approximately 10 times higher than its steady-state level. Such abnormally high Zn concentrations disrupt the function and trafficking of the Zn-dependent chaperone ERp44 at the ER-Golgi interface. In vitro assays using recombinant proteins demonstrated that Zn inhibits the Ero1α-PDI oxidative system, and that ERp44 enhances this inhibitory effect. Consequently, the ER redox environment becomes more reducing, severely impairing the oxidative folding of key membrane receptors such as Notch1 and EGFR. These findings reveal the essential role of zinc homeostasis in redox-dependent proteostasis within the ER. - Source: PubMed
Publication date: 2026/04/22
Amagai YutaArai ChihiroYamamoto WakanaWatanabe SatoshiKowada ToshiyukiSitia RobertoHoseki JunMizukami ShinMatsumoto MasakiInaba Kenji - Zinc, an essential trace element for healthy prostate, which dramatically decreases during prostate tumorigenesis. Targeting the key zinc signaling will be a valuable strategy for PCa therapy. However, the underlying mechanisms are poorly understood. Here, we show that zinc is significantly decreased in prostate cancer (PCa), especially in metastatic PCa. Screening reveals that a zinc transporter Zip7 was upregulated in metastatic PCa and related to poor progression. Zip7 silencing inhibits PCa cell migration and invasion in vitro and bone-metastasis in vivo. Mechanistically, we identify that Zip7 mainly interacts with MAZ in cytoplasm to facilitate MAZ nuclear import and nuclear MAZ was up-regulated in metastatic prostate cancer tissues and positively associated with Zip7 expression, which promotes PCa bone metastasis. Furthermore, our RNA-seq studies reveal that Zip7 facilitates MAZ nuclear import to promote MYBL2 transcription. Strikingly, we show in intraarterial injected-bone metastasis xenograft model that targeting Zip7 by its inhibitor markedly suppressed PCa bone metastasis. Collectively, our findings identify Zip7 is an important regulator of PCa metastasis and targeting Zinc-dependent Zip7-MAZ-MYBL2 could be a valuable strategy to ameliorate advanced PCa metastasis. - Source: PubMed
Publication date: 2026/04/20
Dong QianxiXiong YunqiangXiong SituYuan RuizeLi ShengZhan XiangpengHu HongjiZheng FuchunPang WanFu BinXu SonghuiGuo Ju - Immunonephropathy, encompassing disorders such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD), and membranous nephropathy (MN), is characterized by immune-mediated glomerular injury leading to progressive renal dysfunction. Despite advances in clinical characterization, the precise molecular mechanisms underlying glomerular damage remain poorly understood. - Source: PubMed
Publication date: 2026/03/23
Wu ChengkunYe KengZheng ZiguiXu YanfangChen Zhimin