EPHB4 antibody
- Known as:
- EPHB4 (anti-)
- Catalog number:
- orb101282
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- EPHB4 antibody
Related genes to: EPHB4 antibody
- Gene:
- EPHB4 NIH gene
- Name:
- EPH receptor B4
- Previous symbol:
- HTK
- Synonyms:
- Tyro11
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2016-10-05
Related products to: EPHB4 antibody
Related articles to: EPHB4 antibody
- Periodontitis is traditionally regarded as an oral biofilm-driven inflammatory disease that leads to progressive loss of the tooth-supporting alveolar bone. However, accumulating evidence indicates that periodontal bone loss is more accurately understood as a state of pathological uncoupling of bone remodeling, in which exaggerated bone resorption coexists with inadequate bone formation response. In this review, we reposition periodontitis within the broader context of inflammatory skeletal diseases and synthesize current mechanistic insights from osteoimmunology, bone biology, and mechanobiology. We discuss how excessive osteoclastogenesis in periodontitis is sustained by receptor activator of nuclear factor kappa-B ligand (RANKL) dominance derived from osteocytes, osteoblast-lineage cells, stromal cells, monocytes/macrophages, B and T lymphocytes, and neutrophils within a cytokine-rich microenvironment characterized by tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-17A signaling. Persistent activation of nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways further enhance osteoclast differentiation, survival, and resorptive activity. At the same time, inflammatory mediators actively suppress osteoblast-lineage commitment by inhibiting Runx2 and Osterix, antagonizing canonical Wnt/β-catenin signaling through the upregulation of sclerostin and Dickkopf-1 (DKK1), and impairing bone matrix production and mineralization. We further examine how disruption of key osteoclast-osteoblast coupling mechanisms, including ephrinB2/EphB4 and semaphorin signaling, prevents the effective transition from resorption to formation, while osteocyte dysfunction amplifies the uncoupled phenotype by integrating inflammatory and mechanical signals. Comparisons with rheumatoid arthritis, inflammatory bowel disease-associated bone loss, and peri-implantitis reveal shared immune-driven mechanisms of remodeling imbalance, whereas the unique features of alveolar bone, including high turnover, continuous mechanical loading, and chronic microbial exposure, make it particularly susceptible to inflammatory uncoupling. Together, these concepts support a therapeutic shift toward restoring physiological coupling instead of solely inhibiting resorption and position periodontitis as a clinically accessible model for understanding and targeting inflammatory bone loss across skeletal diseases. - Source: PubMed
Publication date: 2026/07/06
de Molon Rafael ScafTetradis SotiriosVernal RolandoLeite Fabio Renato ManzolliVan Dyke Thomas E - Dental pulp pathologies impair quality of life and systemic health. Obstacles to revascularization remain a key challenge in regenerating dental pulp tissue. To address these challenges, dual-engineered extracellular vesicles (EVs) were developed, incorporating EphrinB2 as a pro-regenerative payload alongside the DNA aptamer Apt02 for endothelial-targeting specificity. This study identified 1 µg/mL as the optimal concentration for fabricating EphrinB2-loaded extracellular vesicles (B2-EVs). At this concentration, B2-EVs significantly enhanced the proliferation, migration, and capillary morphogenesis of HUVECs. Subsequent integration of the endothelial-targeting Apt02 yielded Apt-B2-EVs, which demonstrated superior affinity for HUVECs and amplified pro-angiogenic capacity. Mechanistic analyses confirmed that Apt-B2-EVs promote angiogenesis via the EphrinB2/EphB4-dependent Akt/ERK signaling cascade. These vesicles were further encapsulated within methacrylated gelatin (GelMA) hydrogel, exhibiting sustained release kinetics and excellent biocompatibility. Implantation of Apt-B2-EVs@GelMA into root canals established pulp organoids, which, upon ectopic transplantation in nude mice, robustly enhanced vascularization. The dual-engineered Apt-B2-EVs present a potent strategy for recruiting endothelial cells and delivering EphrinB2 to enable functional pulp revascularization within root canal niches, laying a translational foundation for next-generation functional pulp regeneration. - Source: PubMed
Publication date: 2026/06/30
Liu AnqiLi MengyingTang PeiyuGe WeiwenHan ZhengliangDai YigeZhang LeiYuan ChangyongQi Lei - The MYC oncoprotein drives aggressive tumor behavior across many cancer types, yet its intrinsically disordered structure has limited direct pharmacologic targeting. Building on our previous kinome-wide CRISPR screen, we identify the receptor tyrosine kinase EphB4 as a druggable synthetic-lethal vulnerability in MYC-driven cancers. Genetic ablation or pharmacologic inhibition of EphB4 selectively triggers robust apoptosis in MYC-activated normal cells and MYC-high triple-negative breast cancer (TNBC) cell lines, while sparing MYC-low counterparts. This apoptotic response is Bcl-2-sensitive and p53-independent, overcoming a major resistance barrier in TNBC. In vivo, EphB4 inhibition markedly suppresses MYC-driven tumor growth. Notably, co-targeting EphB4 and Bcl-2 with ABT-199 yields synergistic apoptosis and induces tumor regression in TNBC models. Mechanistically, EphB4 inhibition leads to the selective transcriptional repression of PSMB5, the β5 catalytic subunit of the proteasome, resulting in the impairment of proteasome activity and the induction of MYC-dependent apoptotic stress. This establishes an unexpected link between EphB4 signaling and proteostasis maintenance, a heightened dependency in MYC-overexpressing cells due to their elevated biosynthetic load. Targeting PSMB5 transcription, rather than its catalytic active site, also provides a potential strategy to circumvent or delay resistance to conventional proteasome inhibitors. Together, these findings define the EphB4-PSMB5 axis as a mechanistically distinct and therapeutically actionable vulnerability in MYC-high TNBC, positioning EphB4 inhibition as a promising approach to treat MYC-driven cancers. - Source: PubMed
Publication date: 2026/06/26
Sun ZheZhang YuanYe MengWang ZixinPan ZelinGuo XinZhang ZihengWu RuiWu YeZhang WeidongLuan Xin - Capillary malformation-arteriovenous malformation syndrome is a rare spectrum of vascular anomalies characterized by capillary malformations and high-flow vascular malformations, caused by loss-of-function mutations in the RASA1 and/or EPHB4 genes. These mutations disrupt vascular differentiation and lead to complex malformations involving the brain, skin, and systemic vasculature. Since the first description in 2003, more than 200 cases have been reported, but intracranial arteriovenous shunts during the neonatal period remain extremely rare, as well as reports of the dual mutation RASA1 + EPHB4 or the immunological impact of the EPHB4 mutation. We report three cases of neonates presenting with early-onset high-flow shunts, each exhibiting a distinct genetic signature: CM-AVM1 (RASA1 mutation), CM-AVM2 (EPHB4 mutation), and dual variant (combined EPHB4 and RASA1 mutations). We analyzed and compared the clinical evolution, Doppler ultrasound trends, EEG, MRI and genetic data to highlight the distinct genotype-phenotype spectrum. Early multimodal hemodynamic evaluation of neonates with CM-AVM allows the identification and optimum management of life-threatening shunts at the earliest possible stage. - Source: PubMed
Publication date: 2026/06/14
Nedelcu CarminaCirstoveanu CatalinFilip CristinaStefan Ruxandra IoanaBizubac Ana MihaelaHeriseanu Mariana CarmenDimitriu Mihai C TIonescu Nicolae SebastianAxente Mihaela - Homoharringtonine (HHT) is a purified alkaloid compound isolated from the plant Cephalotaxus, traditionally used in Chinese medicine for various ailments, including leukemia. However, the specific role and biological mechanisms by which HHT regulates metastasis in pancreatic cancer (PC) remain unclear. PC is notorious for its high metastatic potential, yet our understanding of the molecular mechanisms driving its metastasis is still limited. The primary aim of this study is to explore the antimetastatic potential of HHT in PC and elucidate its mechanism of inhibiting epithelial-mesenchymal transition (EMT) via EphB4 and SRI. - Source: PubMed
Publication date: 2026/06/19
Sarwar AmmarZhu ZerenTang XiaoyuTang WenjunCheng YumengTang WenjuanSu QiYang TianfengZhang YanminShi XianpengZhu ManZhang Zixi