EphB1 Control Peptide
- Known as:
- EphB1 Control Peptide
- Catalog number:
- AP14294CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EphB1 Control Peptide
Related genes to: EphB1 Control Peptide
- 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 Control Peptide
Related articles to: EphB1 Control Peptide
- Diabetic kidney disease (DKD) is characterized by heterogeneous renal histological patterns, among which interstitial fibrosis and tubular atrophy (IFTA) is a key determinant of patient outcomes and treatment response. However, blood biomarkers reflecting IFTA burden remain unestablished. - Source: PubMed
Publication date: 2026/08/21
Han Seung SeokSurapaneni Aditya LSchmidt Insa MYun DonghwanMa XufanMoon Kyung ChulSrivastava AnandPalsson RagnarStillman Isaac EWaikar Sushrut SGrams Morgan ERhee Eugene P - 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