Ask about this productRelated genes to: FXYD7 Blocking Peptide
- Gene:
- FXYD7 NIH gene
- Name:
- FXYD domain containing ion transport regulator 7
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2015-07-22
Related products to: FXYD7 Blocking Peptide
Related articles to: FXYD7 Blocking Peptide
- Despite the remarkable success of immune checkpoint inhibitor (ICI) therapy in solid tumors, immune-related adverse events (irAEs) have posed great challenges in the whole-course management of ICI immunotherapy. Reliable biomarkers helping to predict irAEs are still limited and lacking. - Source: PubMed
You LitingZhai JianzhaoXin ZhaodanNa FeifeiWen YangLi JinSong JiajiaBai LingZhou XiaohanYing BinwuZhou Juan - Hippocampal neurogenesis in the dentate gyrus persists into adulthood and plays a crucial role in learning and memory. Early-life exposure to low-dose propofol has been reported to enhance neural development in rodent models, but detailed mechanisms remain unclear. To address this gap, we aimed to investigate how low-dose propofol alters neurogenic lineage differentiation, transcriptional programs, and underlying molecular mechanisms within the early postnatal hippocampal neurogenic niche. : We conducted an in-depth re-analysis of a published single-nucleus RNA-sequencing (snRNA-seq) dataset from hippocampal tissue of postnatal day 10 (PND10) mice, collected 3 days after low-dose propofol treatment. Uniform Manifold Approximation and Projection (UMAP)-based clustering revealed twelve major cell types, including a population of immature pyramidal neurons (imPYR), lacking the mature markers and . Trajectory analysis revealed two neurogenic lineages (granule and pyramidal) and indicated that propofol biases progenitor fate commitment towards the granule lineage. CellChat analysis demonstrated that propofol enhances Neurexin (Nrxn) signaling to neural progenitor cells, suggesting increased synaptic adhesion and maturation. Differential expression analysis (|logFC| ≥ 0.26, adjusted < 0.01) followed by pathway enrichment revealed that propofol upregulates neurogenic maturation pathways-including synaptogenesis, synaptic transmission, dendritic morphogenesis, and memory-related processes-specifically within neural intermediate progenitor cells (nIPC). Together, these findings delineate a coordinated transcriptional and intercellular mechanism by which low-dose propofol reprograms hippocampal neurogenesis during early postnatal development, highlighting progenitor-specific and synapse-oriented processes that may underlie its cognitive-enhancing effects. - Source: PubMed
Publication date: 2025/11/18
Zhang WenLan LiangtianXu XuanxianChen KeyuYang XiaoyuFeng XiaLu Dihan - Advancements in AI-powered systems medicine have revolutionized biomarker discovery through emergent and explainable features. By use of complex network dynamics and graph-based machine learning, we identified critical determinants of lineage-specific plasticity across the single-cell transcriptomics of pediatric high-grade glioma (pHGGs) subtypes: IDHWT glioblastoma and K27M-altered diffuse midline glioma. Our study identified network interactions regulating glioma morphogenesis via the tumor-immune microenvironment, including neurodevelopmental programs, calcium dynamics, iron metabolism, metabolic reprogramming, and feedback loops between MAPK/ERK and WNT signaling. These relationships highlight the emergence of a hybrid spectrum of cellular states navigating a disrupted neuro-differentiation hierarchy. We identified transition genes such as DKK3, NOTCH2, GATAD1, GFAP, and SEZ6L in IDHWT glioblastoma, and H3F3A, ANXA6, HES6/7, SIRT2, FXYD6, PTPRZ1, MEIS1, CXXC5, KDM4C, and NDUFAB1 in K27M subtypes. We also identified MTRNR2L1, GAPDH, IGF2, FKBP variants, and FXYD7 as transition genes (plasticity signatures) that influence cell fate decision-making across both subsystems. We also discovered hub genes such as ITM2C, NOP16, ACTB in IDHWT, and MTRNR2L1, EEF1A1, RPS3A, and H3F3A in K27M gliomas, which serve as central regulators of glioma plasticity and potential therapeutic targets. Our findings suggest pHGGs are developmentally trapped in states exhibiting maladaptive behaviors, and hybrid cellular identities. In effect, tumor heterogeneity (metastability) and plasticity emerge as stress-response patterns to immune-inflammatory microenvironments and oxidative stress. Furthermore, we show that pHGGs are steered by developmental trajectories from radial glia predominantly favoring neocortical cell fates, in telencephalon and prefrontal cortex (PFC) differentiation. By addressing underlying patterning processes and plasticity networks as therapeutic vulnerabilities, our findings provide precision medicine strategies aimed at modulating glioma cell fates and overcoming therapeutic resistance. We suggest transition therapy toward neuronal-like lineage differentiation as a potential precision therapy to help stabilize pHGG plasticity and aggressivity. - Source: PubMed
Publication date: 2025/08/22
Uthamacumaran Abicumaran - The FXYD family of ion transport regulators have emerged as important modulators of cancer progression and metastasis. However, their expression and roles in ovarian cancer (OCa) have not been systematically investigated. - Source: PubMed
Publication date: 2023/10/09
Zhao EryongGao KefeiXiong JianLiu ZhihongChen YuelinYi Lisha - Mechanical allodynia (MA) is the main reason that patients with diabetic peripheral neuropathy (DPN) seek medical advice. It severely debilitates the quality of life. Investigating hyperglycemia-induced changes in neural transcription could provide fundamental insights into the complex pathogenesis of painful DPN (PDPN). Gene expression profiles of physiological dorsal root ganglia (DRG) have been studied. However, the transcriptomic changes in DRG neurons in PDPN remain largely unexplored. In this study, by single-cell RNA sequencing on dissociated rat DRG, we identified five physiological neuron types and a novel neuron type MAAC ( ) in PDPN. The novel neuron type originated from peptidergic neuron cluster and was characterized by highly expressing genes related to neurofilament and cytoskeleton. Based on the inferred gene regulatory networks, we found that activated transcription factors and in MAAC could enhance expression. Moreover, we constructed the cellular communication network of MAAC and revealed its receptor-ligand pairs for transmitting signals with other cells. Our molecular investigation at single-cell resolution advances the understanding of the dynamic peripheral neuron changes and underlying molecular mechanisms during the development of PDPN. - Source: PubMed
Publication date: 2022/05/20
Zhou HanYang XiaoshengLiao ChenlongChen HongjinWu YiweiXie BinranMa FukaiZhang WenChuan