Ask about this productRelated genes to: FXYD1 antibody
- Gene:
- FXYD1 NIH gene
- Name:
- FXYD domain containing ion transport regulator 1
- Previous symbol:
- PLM
- Synonyms:
- -
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-30
- Date modifiied:
- 2016-10-05
Related products to: FXYD1 antibody
Related articles to: FXYD1 antibody
- Recurrent miscarriage (RM) is a prevalent pregnancy complication with incompletely understood molecular mechanisms. Our prior work identified FXYD1 as a hub gene dysregulated in RM and its involvement in decidualization. Thus, this study aimed to characterize the functional role of FXYD1 in trophoblast biology and investigate a FXYD1-centered regulatory axis. - Source: PubMed
Publication date: 2026/08/20
Gan JieYang Shu-HanShi YanZhang YuLian Wen-BoShi Jia-XinZhang ChenZhang XuanWang Jian - Epigenetic silencing of tumor suppressor genes is a hallmark of cancer progression. The FXYD (FXYD domain-containing ion transport regulator) family, classically known for ion transport regulation, has recently been implicated in oncogenesis; however, the role of its founding member, FXYD1, in breast cancer remains unclear. Here, FXYD1 is identified as a significantly downregulated gene in breast cancer tissues, and low FXYD1 expression is associated with unfavorable patient prognosis. Integrative transcriptomic, clinical, and epigenetic analyses revealed that promoter hypermethylation drives FXYD1 silencing. Functional restoration of FXYD1 suppressed cell proliferation, migration, and lung metastasis both in vitro and in vivo. Mechanistically, FXYD1 acts as a nuclear scaffold that recruits the E3 ubiquitin ligase MAEA to the RNA helicase DDX5, a coactivator of β-catenin, promoting K63-linked ubiquitination and proteasomal degradation of DDX5. This process reduces β-catenin stability, impairs its nuclear translocation, and attenuates Wnt target gene expression. Collectively, our findings uncover a previously unrecognized FXYD1-MAEA-DDX5 axis that inhibits Wnt/β-catenin signaling through a non-canonical ubiquitin-proteasome pathway, establishing FXYD1 as a tumor suppressor and potential prognostic biomarker and therapeutic target in breast cancer. - Source: PubMed
Publication date: 2026/03/04
Wen PingQu FanliWang LongShao QingLi SisiQin YangJiang DongpingZhang SenmiaoSui JiangdongWang GuanwenZhang NingningZeng Xiaohua - Breast cancer remains a major global health challenge with high incidence and mortality rates among women. Recent studies have highlighted the critical role of the tumor microenvironment, particularly cancer-associated fibroblasts (CAFs), in tumor progression. However, current understanding of CAFs heterogeneity and its implications for breast cancer diagnosis and treatment remains limited. This study aimed to identify and validate refined marker genes for CAFs and to develop a diagnostic model to improve breast cancer diagnosis and therapeutic strategies. We employed various machine learning algorithms to identify feature genes associated with CAFs. Based on these genes, we constructed a high-precision diagnostic model for breast cancer. Furthermore, through single-cell analysis, we delved into the heterogeneity of CAFs and predicted the sensitivity of different CAF subsets to specific drugs. To validate the expression of these characteristic genes, immunohistochemical (IHC) experiments were also conducted. This study used machine learning to identify FXYD1, SULF1, and TNXB as refined biomarkers for CAFs in breast cancer. Among these evaluated algorithms, the Random Forest algorithm distinctly stood out as the best due to its robust classification accuracy and stability. Single-cell analysis provided insights into the heterogeneity of CAFs between Luminal and non-Luminal breast cancer, thereby enhancing our understanding of the tumor microenvironment. Drug sensitivity predictions indicated that distinct CAF subsets responded differently to specific drugs, laying a solid foundation for the development of personalized breast cancer treatment strategies. Through IHC, the expression patterns of these three biomarkers were verified: FXYD1 was expressed in myoepithelial and fibroblasts in normal breast tissue but was significantly absent in breast cancer; SULF1 was upregulated in fibroblasts of breast cancer; while the expression of TNXB did not exhibit notable variations between normal and cancerous tissues. These findings not only highlight the crucial roles played by FXYD1, SULF1, and TNXB in the development of breast cancer, but also uncover the heterogeneity CAFs. Consequently, our research provides a fresh perspective and a solid theoretical basis for advancing both early and precise diagnostic methods, as well as tailored therapeutic strategies. - Source: PubMed
Publication date: 2026/01/14
Zhou XinWang NaShi LingWei DongxinSun XiaoqinShao MingxiuTian LiangGuo XiaolongZhang FangyuanLyu Hui - Polycystic ovary syndrome (PCOS) is a complex endocrine disorder with an unclear epigenetic basis. This study sought to identify critical methylation regulators implicated in PCOS progression and evaluate their therapeutic potential through comprehensive experimental validation. Bioinformatics analysis was performed to screen differentially expressed genes (DEGs) associated with PCOS and methylation regulators from public databases. Intersection analysis revealed PRDM6 as a key methylation regulator among 177 PCOS-related DEGs and 175 known methylation regulators. Further in silico prediction identified 16 PRDM6-correlated DEGs harboring potential post-translational modification (PTM) sites, with functional enrichment analysis linking them to the cAMP signaling pathway, notably involving RAC3, FXYD1, and SSTR2. To validate these findings, we established in vivo PCOS models using dehydroepiandrosterone-induced rats and in vitro models to mimic PCOS-associated insulin resistance using insulin-induced granulosa cells. In the rodent model, PRDM6 expression was significantly downregulated, while lentivirus-mediated PRDM6 overexpression restored serum sex hormone levels (measured by ELISA) and ameliorated ovarian histopathological abnormalities (assessed via hematoxylin-eosin staining). In vitro, PRDM6 upregulation in granulosa cells attenuated insulin-induced hyperproliferation (evaluated by CCK-8 and EdU assays) and suppressed pro-inflammatory responses (quantified by ELISA). Collectively, these results demonstrated that PRDM6 serves as a pivotal methylation regulator in PCOS pathogenesis, with therapeutic relevance in mitigating hormonal dysregulation, ovarian dysfunction, aberrant granulosa cell proliferation, and inflammation. This study provides novel insights into the epigenetic mechanisms underlying PCOS and highlights PRDM6 as a potential therapeutic target. - Source: PubMed
Publication date: 2025/10/06
Qiu MeitingQu JunjieWang JingyunZhi YunqingTeng Xiaoming - The effect of muscle glycogen stores on performance during intense short-duration exercises in humans is unclear. We hypothesized that low initial muscle glycogen levels would impair constant-load intense one-legged knee extensor exercise lasting approximately 5 min and human muscle contractile function, as determined by maximal voluntary contraction (MVC), electrically induced single-twitch maximal force, rate of force development (RFD), and rate of relaxation. Furthermore, alter phosphorylation of the Na/K-ATPase (NKA) regulatory proteins AMPK and FXYD1 indicating attenuated NKA activity. - Source: PubMed
Publication date: 2025/08/15
Thomassen MartinMcKenna Michael JOlmedillas HugoWyckelsma VictoriaBangsbo JensNordsborg Nikolai Baastrup