EPHB1 (SAM Region)
- Known as:
- EPHB1 (SAM Region)
- Catalog number:
- AP05061PU-N
- Product Quantity:
- 250 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EPHB1 (SAM Region)
Related genes to: EPHB1 (SAM Region)
- Gene:
- AMD1 NIH gene
- Name:
- adenosylmethionine decarboxylase 1
- Previous symbol:
- -
- Synonyms:
- SAMDC
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-03
- Date modifiied:
- 2014-11-19
- Gene:
- ANKS6 NIH gene
- Name:
- ankyrin repeat and sterile alpha motif domain containing 6
- Previous symbol:
- SAMD6, ANKRD14
- Synonyms:
- FLJ36928, NPHP16
- Chromosome:
- 9q22.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-19
- Date modifiied:
- 2016-10-05
- Gene:
- CLMP NIH gene
- Name:
- CXADR like membrane protein
- Previous symbol:
- -
- Synonyms:
- ASAM, FLJ22415, ACAM
- Chromosome:
- 11q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2011-01-27
- Date modifiied:
- 2016-10-05
- Gene:
- DDHD2 NIH gene
- Name:
- DDHD domain containing 2
- Previous symbol:
- SAMWD1
- Synonyms:
- KIAA0725, SPG54
- Chromosome:
- 8p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-23
- Date modifiied:
- 2018-11-15
- 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 (SAM Region)
Related articles to: EPHB1 (SAM Region)
- 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 - We propose an autoencoder-based framework for denoising networks estimated from Spatial Transcriptomics (ST) data for cell signaling analysis. Our method consists of an unsupervised encoder-decoder framework for denoising the network adjacency matrix and a supervised framework for cell signaling estimation. We validate our denoising component using the Frobenius norm metric for graphs simulated using the Barabási-Albert (BA) and Erdős-Rényi (ER) models against reconstructions generated using the singular value decomposition (SVD). We then validate the cell signaling estimates generated using the supervised component on real ST data for the Wnt3-Fzd1 and Ephb1-Efnb3 interactions. We report that our framework achieves better adjacency matrix reconstructions for superlinear BA and dense ER graphs and generates cell signaling estimates that are both regionally specific and biologically plausible. An important contribution of this work is the application of neural networks for network-based cell signaling estimation using ST data and the benchmarking of autoencoder versus SVD denoising for different graph models. - Source: PubMed
Publication date: 2026/05/01
Javaid AzkaFrost H Robert - Neuropathic pain after spinal cord injury reflects persistent hyperexcitability in the spinal cord dorsal horn, yet the molecular drivers sustaining this maladaptive state are unknown. Using an antibody microarray of dorsal horn tissue from mice six weeks after cervical contusion spinal cord injury, we found persistent upregulation of Eph-ephrin signaling, including increased EphB1, EphB2 and EphB3 expression and phosphorylation. Reversible chemogenetic inhibition of EphB kinase activity, using an EphB1/2/3 analog-sensitive knock-in mouse, selectively reversed established mechanical allodynia without affecting thermal hyperalgesia or motor function and also shifted dorsal horn signaling away from pain sensitization-associated pathways. Among EphB receptors, EphB2 showed the most consistent and robust injury-induced increase in expression within dorsal horn. Although EphB2 transcript levels increased in both dorsal horn neurons and astrocytes, conditional deletion of EphB2 only in dorsal horn neurons, but not in astrocytes, reversed established mechanical allodynia and reduced dorsal horn neuronal activation. These findings identify EphB signaling, and neuronal EphB2 in particular, as a mechanism that actively maintains pain hypersensitivity after spinal cord injury. - Source: PubMed
Publication date: 2026/04/22
Heinsinger Nicolette MJaffe David ASrikanth Kolluru DLyttle Megan ASmith Madison SThomas Samantha JCharsar Brittany ACheng LanMichel-Flutot PaulineCain Rachel EWatson Jaime LBao DuranFan JiaFalnikar AditiZhou WeiDalva Matthew BLepore Angelo C