EphB4, Mab anti_; Clone AB105
- Known as:
- EphB4, Mab anti_; Clone AB105
- Catalog number:
- AB105-1000
- Product Quantity:
- 1000 ug.
- Category:
- -
- Supplier:
- Accu
- Gene target:
- EphB4 Mab anti_; Clone AB105
Related genes to: EphB4, Mab anti_; Clone AB105
- 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
- Gene:
- GOLGB1 NIH gene
- Name:
- golgin B1
- Previous symbol:
- -
- Synonyms:
- GCP, GCP372, giantin, GOLIM1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-05
- Date modifiied:
- 2016-10-05
- Gene:
- SERPINA1 NIH gene
- Name:
- serpin family A member 1
- Previous symbol:
- PI
- Synonyms:
- AAT, A1A, PI1, alpha-1-antitrypsin, A1AT, alpha1AT
- Chromosome:
- 14q32.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- SERPINB1 NIH gene
- Name:
- serpin family B member 1
- Previous symbol:
- ELANH2
- Synonyms:
- EI, PI2, anti-elastase
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-27
- Date modifiied:
- 2016-04-06
Related products to: EphB4, Mab anti_; Clone AB105
Related articles to: EphB4, Mab anti_; Clone AB105
- - Source: PubMed
Publication date: 2026/07/29
Lin YanyanZhan MinzhenChen XiangqiXiao Xuemin - EphrinB2 and its receptor EphB4 have been reported to play a crucial role in the development of the cardiovascular system, and the process of coronary artery disease (CAD) is closely related to angiogenesis. The aim of this study is to identify and analyze the therapeutic value of the EphrinB2/EphB4 signaling pathway and angiogenesis-related biomarkers. - Source: PubMed
Publication date: 2026/07/20
Liu ChunyuCheng WeiweiWei XingSong DiZhang Zhibiao - 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