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)
- 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 - Gastric cancer (GC) remains a major global health challenge, characterized by high morbidity and mortality rates. Early diagnosis is essential for improving patient outcome. This study aims to develop a diagnostic model based on specific signature genes by investigating the association between double-negative (DN) T cells and GC. - Source: PubMed
Publication date: 2026/01/12
Yin ZhijingZhang GanghuaYin ZiweiMa WeinaYang JingxinDeng WenzhiFeng ZiyangWang ZhanwangJin YiZhu YuxingCao Ke - Pancreatic cancer (PC) is a highly malignant and aggressive gastrointestinal malignancy with a poor prognosis for patients. Aerobic glycolysis serves as a critical metabolic driver of PC progression. Our study aims to elucidate the mechanism by which FXYD5 regulates aerobic glycolysis in PC. - Source: PubMed
Publication date: 2025/09/17
Xie HongminLiao LangxiaLi JiaxuanCai RunshengHe HongBiaoLu Min