FXYD5 antibody - center region (OAAB11244)
- Known as:
- FXYD5 (anti-) - central region (OAAB11244)
- Catalog number:
- oaab11244
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FXYD5 antibody - center region (OAAB11244)
Related genes to: FXYD5 antibody - center region (OAAB11244)
- Gene:
- FXYD5 NIH gene
- Name:
- FXYD domain containing ion transport regulator 5
- Previous symbol:
- -
- Synonyms:
- OIT2
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2014-11-19
Related products to: FXYD5 antibody - center region (OAAB11244)
Related articles to: FXYD5 antibody - center region (OAAB11244)
- Glioblastoma (GBM) is the most malignant primary brain tumor, with limited therapeutic options. Dysregulation of FXYD5 has been reported in multiple malignancies, suggesting FXYD5 as a potential target for precision medicine. In the present study, FXYD5 expression and prognostic significance were analyzed using biological analysis on multiple databases and it was identified that FXYD5 was observably upregulated in GBM and inversely correlated with the prognosis of patients. Functional studies were investigated in LN229 and U251 GBM cell lines through FXYD5 knockdown and overexpression approaches, assessing proliferation (Cell Counting Kit‑8), apoptosis (flow cytometry), migration/invasion (Transwell assays) and lipid metabolism (free fatty acids, triglycerides, cholesterol, Nile Red staining). Knockdown of FXYD5 suppressed GBM cell proliferation, migration and invasion, while increasing apoptosis, indicating that FXYD5 may serve as a therapeutic target for GBM. Mechanistic studies examined the PI3K/AKT/long‑chain acyl‑coenzyme A (CoA) synthase 4 4 (ACSL4) pathway via western blotting and rescue experiments, finding that FXYD5 activated the PI3K/AKT signaling pathway, leading to upregulation of ACSL4 and enhanced lipid metabolism. , a subcutaneous xenograft mouse model was used to evaluate whether PI3K/AKT inhibition could antagonize FXYD5 overexpression‑induced tumor growth and PI3K/AKT inhibition reversed FXYD5 overexpression‑induced tumor growth in the subcutaneous mouse model. These findings revealed that FXYD5 promotes GBM progression via the PI3K/AKT/ACSL4 signaling axis and represents a potential therapeutic target for GBM. - Source: PubMed
Publication date: 2026/09/18
Wang BangQin YongCheng HangZeng YibinJiang LiangleiHu Xuebin - Anterior cruciate ligament (ACL) rupture leads to muscle deconditioning and downregulation of Na,K-ATPase (NKA). Low-load blood flow restriction (LL-BFR) training was shown to improve muscle function after ACL injury, but its effects on NKA are unknown. We analyzed the expression of NKA and its FXYD regulators in knee muscles from ACL-injured subjects undergoing LL-BFR, low-load training with sham blood flow restriction (LL-Sham), or no training (Control). In addition, we dissected effects of ischemia components by subjecting cultured human myotubes to glucose deprivation and/or hypoxia. The LL-BFR group had higher vastus lateralis mRNA levels of NKAα1 than the Control and LL-Sham groups. In vitro, NKAα1, NKAβ1, and NKAβ3 mRNA and NKAα1 and NKAβ1 protein levels were downregulated by sustained ischemia and glucose deprivation, but not hypoxia, whereas FXYD5 protein was upregulated by glucose deprivation. Conversely, intermittent ischemia had no effect on NKA or FXYD expression. In conclusion, LL-BFR training was associated with upregulation of NKAα1 mRNA levels in the vastus lateralis after ACL injury; however, in the absence of corresponding changes in protein abundance, its contribution to functional recovery remains unclear. Moreover, our in vitro findings suggest that glucose availability plays a major role in modulating NKA and FXYD expression in muscle cells under ischemic conditions. This is the first study exploring effects of low-load BFR training on Na,K-ATPase (NKA) and FXYD expression in knee muscles after anterior cruciate ligament injury. Effects of ischemia components were analyzed by subjecting cultured human myotubes to glucose deprivation and/or hypoxia. The LL-BFR group had higher vastus lateralis mRNA levels of NKAα1 than the Control and LL-Sham groups. Glucose plays a major role in modulating NKA and FXYD expression in cultured myotubes under ischemic conditions. - Source: PubMed
Publication date: 2026/09/02
Jan VidMiš KatarinaKacin AlanVidović AnjaTomc Žargi TinaStražar KlemenPodbregar MatejMarš TomažDrobnič MatejChibalin Alexander VPirkmajer Sergej - Spinal cord injury often causes permanent disability because the body's own repair mechanisms are limited, and the molecules that control damage and healing are not fully understood. One such molecule, FK506-binding protein 5 (FKBP5), is known to rise sharply after injury, but whether it only drives harmful inflammation or also participates in later recovery has been unclear. In this study, we investigated how FKBP5 affects microglia-the brain's immune cells-at different stages after spinal cord injury in mice. We found that FKBP5 plays a dual role. In the first few days, it works together with another protein, GPR84, to boost the production of an inflammatory signal called interleukin-1β. This signal pushes microglia into a destructive state and triggers a coordinated form of neuronal cell death that involves multiple death pathways. However, as FKBP5 levels continue to rise over time, it switches its function. It binds to and modifies an enzyme called LDHA, changing how microglia process lactate. This lactate then acts as a signal to add chemical tags (lactylation) onto histones, which turns on a protective gene, Fxyd5, and its partner Lgals1. These changes convert microglia from a harmful to a healing state, reduce neuronal death, and improve the local environment for tissue repair. Our results reveal that FKBP5 is a double-edged sword-first worsening damage, then promoting repair. This discovery suggests that precisely timing therapies that target FKBP5 could offer a new way to improve recovery after spinal cord injury. - Source: PubMed
Publication date: 2026/08/04
Li HaotianWang JingLi DaohuiBi HangchuanYang JinDong JunjieGong ZhiqiangGong HongdaWang BingChen Lingqiang - Papillary thyroid cancer is one of the most common malignancies in pediatrics, with increasing prevalence. We analyzed the single-cell transcriptomic landscape from 11 pediatric patients. The compositions and functions in the tumor microenvironment showed remarkable differences. Endo_tip was primarily from tumor, receiving angiogenesis-associated signals from epithelia. Abundant immune cells infiltrated into tumor. SPP1+ M2-macrophage and tumor cells interacted with T cells via immunosuppressive ligand-receptor pairs. Trajectory inference identified genes in evolutionary branchpoints that may participate in tumor progression. Analyzing the correlation of genes with thyroid differentiation score, clinicopathological features, and prognosis, we identified that FXYD5 might play a key role. RNA-seq data showed FXYD5 mediated proliferation and migration via apoptosis and adhesion processes. Compared with adults, epithelia in pediatrics exhibit higher enrichment in tumor-associated pathways; however, the differences in tumor microenvironment are less pronounced. Our findings reveal a heterogeneous microenvironment of pediatric PTC and identify FXYD5 as a potential prognostic and therapeutic marker. - Source: PubMed
Publication date: 2026/06/26
Yu JuLin BoChen WannaTang QinZheng LiangLiang XiaoliWang FangPeng SuiLiu YihaoLi JieLiu RengyunXiao HaipengLv Weiming - Erythro-myeloid progenitors (EMPs) originate from the haemogenic endothelium in the yolk sac via an endothelial-to-haematopoietic transition (EHT) to generate blood and immune cells that support embryo development. Yet, the transitory nature of EHT and the limited availability of molecular markers have constrained our understanding of the origin, identity, and differentiation dynamics of EMPs. Here, we have refined the annotation of yolk sac haemato-vascular populations in publicly available single-cell RNA sequencing (scRNAseq) datasets from mouse embryos to identify novel molecular markers of haemogenic endothelium and EMPs. By sub-clustering key cell populations followed by pseudotime analysis, we refined cluster annotations and then reconstructed differentiation trajectories. Subsequent differential gene expression analysis between clusters identified novel cell surface markers for haemogenic endothelial cells ( and ) and EMPs (, and ). Further, we have identified candidate signalling and metabolic pathways that may regulate yolk sac haematopoietic emergence and differentiation. The specificity of FXYD5, SCARF1, and FCER1G for haemogenic endothelium and EMPs was validated by immunostaining of the mouse yolk sac. These insights into the transcriptional dynamics in the yolk sac should support future investigation of EHT and haematopoietic differentiation during early mammalian development. - Source: PubMed
Publication date: 2026/01/06
Diez-Pinel GuillermoMuratore AlessandroRuhrberg ChristianaCanu Giovanni