Ask about this productRelated genes to: SLC39A5 antibody
- Gene:
- SLC39A5 NIH gene
- Name:
- solute carrier family 39 member 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-08
- Date modifiied:
- 2016-02-17
Related products to: SLC39A5 antibody
Related articles to: SLC39A5 antibody
- Methylation of histidine residues in zinc transporters by histidine methyltransferase METTL9 plays an important role in modulating their metal-binding properties. Here, we report synthetic, enzymatic, and computational studies on human METTL9-catalyzed Nπ-methylation of His375 in zinc transporter SLC39A5-derived peptides in which the histidine substrate and its neighboring residues are substituted by chemically and structurally diverse proteinogenic and nonproteinogenic amino acids. Our work reveals that the xHxH motif (residues 372-375) is essential for efficient Nπ-histidine methyltransferase METTL9 catalysis. We demonstrate that human METTL9 has an exceptionally narrow substrate scope towards His375 and does not catalyze methylation of simple histidine mimics in the SLC39A5 peptide. Moreover, METTL9 recognizes only 2-pyridylalanine, 3-(4-thiazolyl)alanine and backbone N-methylated histidine residues at position 373 in addition to the natural His373 residue. METTL9 has also a capacity to recognize a few simplest mimics of Ser374 and Gly372 residues in the SLC39A5 sequence. Molecular dynamics simulations support the experimental findings and deliver a comprehensive structural basis on the significance of the xHxH motif for stable METTL9-SLC39A5 complex formation and efficient METTL9 catalysis. Overall, this study provides evidence for different substrate selectivities of human histidine methyltransferase METTL9, the knowledge important from basic molecular and biomedical perspectives. - Source: PubMed
Ahmad SadafMoesgaard LaustTornøe Christian WEmmel PaulinaSlusarczyk KlaudiaDrozak JakubKongsted JacobMecinović Jasmin - Glucagon is a critical regulator of glucose homeostasis by regulating liver glycogenolysis and gluconeogenesis. Hyperglucagonemia has been observed in patients with type 2 diabetes mellitus (T2DM). However, whether elevated glucagon is cause or consequence in the pathogenesis of T2DM is poorly investigated. - Source: PubMed
Publication date: 2025/11/10
Chen WenliCui WeiyiXu YanWang XuelianSun XuetingRen JingHou NingXiong WenyongXiao Rui-PingZhang Xiuqin - Despite advances in diagnostic and therapeutic methods for gastric cancer (GC), early detection continues to be a significant challenge, resulting in late-stage diagnoses and poor survival outcomes. Studies have shown that solute carrier family 39 member 5 (SLC39A5) is upregulated in GC and may serve as a potential prognostic biomarker. However, the exact role of SLC39A5 and its underlying mechanisms remains unclear. To evaluate cell proliferation, migration, and invasion, a variety of assays, including Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine incorporation, scratch, and Transwell assays, were conducted. The molecular interactions among genes were investigated through coimmunoprecipitation, chromatin immunoprecipitation, and dual luciferase reporter assays. An in vivo GC mouse model was established to substantiate our in vitro findings. Knockdown of SLC39A5 inhibited GC cell proliferation, migration, and invasion. Furthermore, SLC39A5 increased Moloney murine leukemia virus 1 (proto-oncogene serine/threonine-protein kinase 1 [PIM1]) kinase activity by enhancing zinc influx, which in turn triggered basic leucine zipper ATF-like transcription factor (BATF) phosphorylation and stabilized BATF protein. BATF overexpression reversed the inhibitory effect of SLC39A5 depletion on the behavior of GC cells and tumor growth. Moreover, we found that BATF, combined with the Jun proto-oncogene, AP-1 transcription factor subunit (JUN), led to the suppression of Huntingtin interacting protein 1-related (HIP1R) expression and the activation of the PI3K/protein kinase B (AKT) pathway. In conclusion, SLC39A5 promotes the progression of GC via the BATF-HIP1R axis, which suggests that SLC39A5 acts as a therapeutic or diagnostic target for GC. - Source: PubMed
Publication date: 2025/09/22
Wang XinyuLi TaoXia MingxiSun LeichaoWang Xudong - To investigate the variants in 18 disease-causing genes associated with nonsyndromic myopia in 83 Chinese individuals diagnosed with early-onset high myopia(eo-HM). - Source: PubMed
Publication date: 2025/09/08
Liu YangZhang Shao-ChiZhang WenXue Zhong-QiQin Yi-XuanPiao Shun-YuLi Wen-JingJi Meng-LiZhuang Wen-Juan - Recent studies have revealed a role for zinc in insulin secretion and glucose homeostasis. Randomized placebo-controlled zinc supplementation trials have demonstrated improved glycemic traits in patients with type II diabetes (T2D). Moreover, rare loss-of-function variants in the zinc efflux transporter reduce T2D risk. Despite this accumulated evidence, a mechanistic understanding of how zinc influences systemic glucose homeostasis and consequently T2D risk remains unclear. To further explore the relationship between zinc and metabolic traits, we searched the exome database of the Regeneron Genetics Center-Geisinger Health System DiscovEHR cohort for genes that regulate zinc levels and associate with changes in metabolic traits. We then explored our main finding using in vitro and in vivo models. We identified rare loss-of-function (LOF) variants (MAF <1%) in () associated with increased circulating zinc (p=4.9 × 10). Trans-ancestry meta-analysis across four studies exhibited a nominal association of LOF variants with decreased T2D risk. To explore the mechanisms underlying these associations, we generated mice lacking mice display improved liver function and reduced hyperglycemia when challenged with congenital or diet-induced obesity. These improvements result from elevated hepatic zinc levels and concomitant activation of hepatic AMPK and AKT signaling, in part due to zinc-mediated inhibition of hepatic protein phosphatase activity. Furthermore, under conditions of diet-induced non-alcoholic steatohepatitis (NASH), mice display significantly attenuated fibrosis and inflammation. Taken together, these results suggest SLC39A5 as a potential therapeutic target for non-alcoholic fatty liver disease (NAFLD) due to metabolic derangements including T2D. - Source: PubMed
Publication date: 2024/12/13
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