SLC39A7 antibody - N-terminal region (ARP43812_P050)
- Known as:
- SLC39A7 (anti-) - N-terminal region (ARP43812_P050)
- Catalog number:
- arp43812_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SLC39A7 antibody - N-terminal region (ARP43812_P050)
Related genes to: SLC39A7 antibody - N-terminal region (ARP43812_P050)
- 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 - N-terminal region (ARP43812_P050)
Related articles to: SLC39A7 antibody - N-terminal region (ARP43812_P050)
- : 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 - 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 - Proteins can be methylated at either of the two N atoms of the imidazole ring of histidine, yielding 1-methylhistidine (or pi-methylhistidine) or 3-methylhistidine (tau-methylhistidine). While protein histidine methylation in mammals was discovered more than 50 years ago, the first histidine methyltransferases were identified only recently. So far, four different human protein histidine methyltransferases have been uncovered, and one of these is METTL9, which is responsible for introducing 1-methylhistidine in a number of proteins. The minimal sequence motif that is required, though not always sufficient, for METTL9-mediated methylation is His-X-His (HxH), where X is preferentially a small uncharged residue. Many METTL9 substrates are methylated at stretches of alternating histidines, i.e., several adjoining HxH motifs, such as HxHxH. Histidines are frequently involved in binding metal ions, such as zinc. Accordingly, it has been shown for several sequences targeted by METTL9, for example, in the immunomodulatory and antibacterial protein S100A9 and the zinc transporter SLC39A7, that histidine methylation diminishes zinc binding and thereby modulates protein function. In this review, we present a detailed account of METTL9-mediated histidine methylation, regarding its discovery, biochemical mechanism, structural features, and biological significance. - Source: PubMed
Publication date: 2026/03/09
Falnes Pål ØDavydova Erna - Osteoporosis is a prevalent systemic metabolic disease, and an imbalance in the adipogenic and osteogenic differentiation of mesenchymal stem cells (MSCs) plays a crucial role in its pathogenesis. Thus, elucidating the mechanisms that regulate MSC lineage allocation is urgently needed. METTL9 was recently characterized as a novel N1-histidine methyltransferase that performs a wide range of functions. however, the role of METTL9 in the imbalance of MSC differentiation in osteoporosis remains unclear. In this study, we found that METTL9 expression was downregulated in osteoporosis, and further adipogenic functional experiments revealed that METTL9 negatively regulated the adipogenic differentiation of MSCs both in vitro and in vivo. Mechanistically, METTL9 mediated methylation of SLC39A7 at the His45 and His49 residues suppressed ferroptosis through the endoplasmic reticulum (ER) stress regulatory protein kinase R-like endoplasmic reticulum kinase (PERK)/ATF4 signaling pathway and the downstream protein SLC7A11. Moreover, SLC7A11 transported cystine for intracellular glutathione synthesis, eliminating intracellular reactive oxygen species (ROS) and inhibiting MSC adipogenic differentiation. Additionally, METTL9 overexpression significantly alleviated bone loss in ovariectomy (OVX) model mice. In summary, our results suggest that the METTL9/SLC39A7 axis may be a promising diagnostic and therapeutic target for osteoporosis. - Source: PubMed
Publication date: 2025/05/26
Jin JiahaoLi QuanfengZhang YunhuiJi PengfeiWang XinlangZhang YibinYuan ZihaoJiang JiananTian GuangqiCai MingxiFeng PeiWu YanfengWang PengLiu Wenjie - Intervertebral disc degeneration (IVDD) is a prevalent condition contributing to various spinal disorders, posing a significant global health burden. Mitophagy plays a crucial role in maintaining mitochondrial quantity and quality and is closely associated with the onset and progression of IVDD. Well-documented region-specific mitophagy mechanisms in IVDD are guiding the development of therapeutic strategies. In the nucleus pulposus (NP), impaired mitochondria lead to apoptosis, oxidative stress, senescence, extracellular matrix degradation and synthesis, excessive autophagy, inflammation, mitochondrial instability, and pyroptosis, with key regulatory targets including AMPK, PGC-1α, SIRT1, SIRT3, Progerin, p65, Mfn2, FOXO3, NDUFA4L2, SLC39A7, ITGα5/β1, Nrf2, and NLRP3 inflammasome. In the annulus fibrosus (AF), mitochondrial damage induces apoptosis and oxidative stress mediated by PGC-1α, while in the cartilage endplate (CEP), mitochondrial dysfunction similarly triggers apoptosis and oxidative stress. These mechanistic insights highlight therapeutic strategies such as activating Parkin-dependent and Ub-independent mitophagy pathways for NP, enhancing Parkin-dependent mitophagy for AF, and targeting Parkin-mediated mitophagy for CEP. These strategies include the use of natural ingredients, hormonal modulation, gene editing technologies, targeted compounds, and manipulation of related proteins. This review summarizes the mechanisms of mitophagy in different regions of the intervertebral disc and highlights therapeutic approaches using mitophagy modulators to ameliorate IVDD. It discusses the complex mechanisms of mitophagy and underscores its potential as a therapeutic target. The objective is to provide valuable insights and a scientific basis for the development of mitochondrial-targeted drugs for anti-IVDD. - Source: PubMed
Publication date: 2025/04/01
Feng ChaoqunHu ZiangZhao MinLeng ChuanLi GuangyeYang FeiFan Xiaohong