EphB4, Mab anti-; Clone: AB105
- Known as:
- EphB4, Mab (anti-) to-; Clone: AB105
- Catalog number:
- ab105-200
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Accurate
- 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
- Radiotherapy eliminates most tumor cells but spares persister tumor cells that evade cell death and drive relapse. Increasing evidence suggests that stromal components of the tumor microenvironment influence treatment responses, yet whether macrophages actively reprogram tumor-intrinsic stress responses to promote radioresistance remains unclear. Here, we investigated the mechanisms by which macrophage-tumor cell interactions regulate ferroptosis and tumor survival after irradiation. We used macrophage-tumor cell coculture systems, Transwell separation assays, and 3D microfluidic models to examine contact-dependent effects on tumor survival following irradiation. Kinome-wide small interfering RNA screening, RNA sequencing, lipidomic profiling, and quantitative proteomic analysis of secretomes were performed to identify signaling pathways and metabolic changes. Genetic and pharmacological perturbation of Ephrin receptor b4 (Ephb4) signaling were evaluated in vitro and in syngeneic mouse tumor models. Clinical relevance was assessed using transcriptomic analyses and immunohistochemical staining of patient tumor specimens. Macrophage contact reduced lipid peroxidation and cell death in irradiated tumor cells in a contact-dependent manner. Kinome screening identified Ephb4 as a key mediator induced by irradiation in tumor cells. Ephb4 engagement with ephrinb2 on macrophages initiated bidirectional signaling that increased expression of ferroptosis-protective genes (solute carrier family 7 member [], solute carrier family 3 member 2 [], and glutathione peroxidase 4 []) in tumor cells while activating the toll-like receptor 2- nuclear factor-kappa B pathway and interleukin-6 (IL-6) production in macrophages. Macrophage-derived IL-6 further sustained ferroptosis resistance in tumor cells, and Ephb4-driven secretion of cathepsin S amplified macrophage IL-6 production through a feedforward loop. Genetic or pharmacological inhibition of Ephb4 restored lipid peroxidation and markedly enhanced radiosensitivity in vitro and in vivo. Analysis of patient datasets demonstrated increased EPHB4 expression following radiotherapy and an association between high EPHB4 expression, reduced ferroptosis signatures, and poor treatment response. These findings identify a macrophage-driven ferroptosis evasion program that enables tumor cell survival after irradiation and demonstrate that Ephb4 coordinates bidirectional tumor-macrophage signaling to sustain this resistance. Targeting the Ephb4-ephrinb2 axis represents a potential strategy to enhance ferroptosis and improve radiotherapy efficacy in resistant tumors. - Source: PubMed
Publication date: 2026/09/04
Chung HyewonKim Sang WhaOh Jae WonPark Gyu MiCho YurimChoi Hae SukKim MinJiKim Kwang PyoNa Yi RangLee Hye SeungKim Hak JaeSeok Seung Hyeok - Given the distinct pathogenic mechanisms of early-onset Alzheimer's disease (EOAD) and late-onset Alzheimer's disease (LOAD), identifying disease-specific therapeutic targets for each subtype is particularly critical. - Source: PubMed
Publication date: 2026/03/04
Chen LinSun HongxuFang Ming-JuanCheng NanXu Yin - - 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