EphB1 (+EphB2_3_4)
- Known as:
- EphB1 (+EphB2_3_4)
- Catalog number:
- AP21112PU-N
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EphB1 (+EphB2_3_4)
Related genes to: EphB1 (+EphB2_3_4)
- Gene:
- EPHB1 NIH gene
- Name:
- EPH receptor B1
- Previous symbol:
- EPHT2
- Synonyms:
- Hek6
- Chromosome:
- 3q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-23
- Date modifiied:
- 2016-01-15
Related products to: EphB1 (+EphB2_3_4)
Related articles to: EphB1 (+EphB2_3_4)
- BackgroundDifferential expression of long non-coding RNAs (lncRNAs) in brain, serum, and blood show strong potential to distinguish Alzheimer's disease (AD) from healthy controls.ObjectiveTo explore whether lncRNA signatures delineate AD pathology and map to distinct, multidimensional cognitive domains, enhancing specificity in assessing AD severity and progression.MethodsWe profiled 29,603 lncRNAs transcripts in blood samples from 15 AD patients and 15 healthy controls, alongside comprehensive neuropsychological assessments. Generalized Linear Models and Predictive Power Score analyses, with statistical prioritization, identified lncRNAs associated to AD neuropsychological architecture.ResultsSeveral lncRNAs share strongly associated with cognitive performance and AD severity, mapping to genes involved in key AD-related molecular processes, including synaptic and neurotransmitter regulation (e.g., , , ), protein homeostasis and Aβ pathology (e.g., , , ), mitochondrial function and cellular stress (e.g., , ), neuroinflammation and immune regulation (e.g., , , ), epigenetic and transcriptional control (e.g., , , ), neuronal excitability (e.g., ), and neuroprotection and synaptic plasticity (e.g., ). Novel associations included ferroptosis, DNA stability, microtubule dynamics, and dendritic orientation (e.g., , , , , , , ).ConclusionsWe identify candidate lncRNA signatures that may serve as potential biomarkers and enhance our understanding of the molecular basis of the cognitive architecture in AD, opening new avenues for biomarker identification and targeted therapeutic strategies development. Validation in larger, diverse cohorts is essential to confirm their mechanistic contributions to AD. - Source: PubMed
Publication date: 2026/07/29
Mosquera-Heredia María IVidal Oscar MBarceló ErnestoMorales Luis CSilvera-Redondo CarlosBolívar Daniel AAllegri RicardoArcos-Burgos MauricioGaravito-Galofre PilarVélez Jorge I - Circadian disruption affects multiple aspects of human health, but the genetic architecture of individual susceptibility remains unclear. We examined the genetics of the Circadian Imbalance Index (CII), an additive 0-5 score combining evening chronotype, short/long sleep, high neuroticism, atypical caffeinated coffee intake, and low vitamin D. - Source: PubMed
Publication date: 2026/07/21
Żebrowska MagdalenaWielscher MatthiasZhang JingSaksvik-Lehouillier IngvildDiMilia LeeBurns AngusValliere JesseVincenzi LeonardoRedline SusanOkereke OliviaSaxena RichaRichmond RebeccaRutter Martin KSchernhammer Eva S - The treatment of Alzheimer's disease (AD) is severely hampered by the blood-brain barrier (BBB), which limits the delivery of therapeutic agents like donepezil (DPZ), an acetylcholinesterase inhibitor. While DPZ has multi-faceted benefits, its clinical efficacy is constrained by poor BBB penetration, requiring high doses that lead to significant side effects. To overcome this, we developed a brain-targeted nanotherapeutic utilizing apoferritin (AFn) nanoparticles loaded with DPZ (AFn-DPZ). We demonstrate that this platform, by binding to the EphB1 receptor on the blood-brain barrier, enables transient and reversible opening of the blood-brain barrier, thereby facilitating efficient and targeted drug delivery. Following intravenous administration in an AD mouse model, AFn-DPZ exhibited enhanced brain accumulation and sustained release of DPZ. This targeted delivery inhibited acetylcholinesterase activity, reduced amyloid plaque burden, alleviated neuroinflammation, attenuated oxidative damage, restored mitochondrial function, and upregulated the expression of brain-derived neurotrophic factor (BDNF). Consequently, AFn-DPZ treatment significantly improved cognitive performance compared to free DPZ. Our findings establish EphB1-mediated facilitation of BBB traversal as a promising strategy for enhancing nanotherapeutic delivery to the brain, offering a potent approach to address the complex pathology of AD. - Source: PubMed
Publication date: 2026/07/06
Wen ShilinGao JingjingWang ZhixianMa QiuminXu Xiao-LingChen Jianer - Gliosarcoma is a rare and aggressive variant of glioblastoma characterized by biphasic glial and sarcomatous components. Lesions arising from the craniovertebral junction or brainstem are extremely uncommon, and their molecular pathogenesis remains poorly understood. A 69-year-old woman presented with rapidly progressive quadriparesis. Magnetic resonance imaging demonstrated an enhancing mass extending from the clivus to the medulla and an additional lesion in the ventricular trigone. Partial resection via an endoscopic transpharyngeal transclival approach achieved decompression. Histologically, the tumor exhibited distinct glial and sarcomatous components, with loss of H3K27me3 expression restricted to the sarcomatous areas. Comprehensive molecular profiling revealed mutations in PTEN, SUZ12, TERT, and EPHB1. Despite adjuvant radiation therapy, temozolomide, and bevacizumab, leptomeningeal dissemination occurred, and the patient died five months postoperatively. This rare case of gliosarcoma arising at the craniovertebral junction exhibited distinctive molecular and epigenetic features, including a SUZ12 mutation potentially associated with loss of H3K27me3. To our knowledge, gliosarcoma harboring these molecular abnormalities has not been previously reported. These findings may be associated with PRC2 dysfunction; however, their biological significance remains to be clarified. Comprehensive molecular profiling may contribute to improved diagnostic characterization of such rare entities. - Source: PubMed
Publication date: 2026/06/02
Ikemoto TomokoHasegawa HirotakaHana TaijunKanbe MayuMurakami ChiakiImada HirokiHigashi MorihiroHanakita Shunya - Synaptogenesis-related neuron-glioma interactions are increasingly recognized in glioma, yet it remains unclear whether routine H&E morphology can capture these programs and improve prognostic stratification. We integrated H&E whole-slide images, transcriptomes, and clinical data from 434 TCGA gliomas. Deep learning and quantitative pathology yielded an integrated histomorphologic feature set of 2678 features. Synaptogenesis-related activity was quantified using ssGSEA for ninety-eight synaptogenesis-related genes. In the training cohort, Spearman analysis identified 149 correlated histomorphologic features, which were refined to thirty-five by elastic net regularization. Seventeen prognostic candidates were entered into the MIME1 framework, and the most parsimonious model, Enet[0.1], retained fourteen non-zero-coefficient features to define the synaptogenesis-associated histomorphologic signature and construct the pathology-derived risk score (PRS). Multi-omic analyses, Human Protein Atlas validation, and single-nucleus RNA-seq were used to investigate the hub gene and its cellular context. PRS robustly stratified survival in both training and validation cohorts and remained an independent prognostic factor after adjustment for age and 2021 WHO CNS grade. High-risk tumors showed increased stromal and immune scores and enrichment of immune, adhesion, and phagosome-related pathways. emerged as the hub gene and was enriched in glioblastoma, and -positive malignant cells displayed prominent communication with neurons, including EFNB2-EPHB1 signaling. Exploratory re-analysis of the myeloid compartment further showed that glioblastoma was enriched for suppressive TAM-like states relative to astrocytoma grade 2, supporting a shift toward a more tumor-associated and potentially immunosuppressive microenvironment. Routine H&E histomorphology can capture synaptogenesis-related molecular programs in glioma. The resulting PRS provides clinically relevant prognostic stratification, while -positive malignant cells may represent a candidate hub for neuron-tumor communication within a remodeled tumor ecosystem. - Source: PubMed
Publication date: 2026/05/12
Wu XiaolongLiu DongGeng HaomingZhang BinghanDiao HuantongZhou YiqiangSong GangCheng YeLiang Jiantao