EphB4, Mab anti-; Clone: AB107
- Known as:
- EphB4, Mab (anti-) to-; Clone: AB107
- Catalog number:
- ab107-1000
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Accurate
- Gene target:
- EphB4 Mab anti-; Clone: AB107
Related genes to: EphB4, Mab anti-; Clone: AB107
- 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: AB107
Related articles to: EphB4, Mab anti-; Clone: AB107
- Postmenopausal osteoporosis is driven by estrogen-deficiency-associated uncoupling of bone formation and resorption. This study quantified the independent and interactive effects of Zuogui Pill Yin-nourishing subformulations in an ovariectomized rat model and examined associations with the EphB4/ephrinB2/RhoA/alkaline phosphatase pathway. In accordance with ARRIVE 2.0, 130 specific pathogen-free female Sprague-Dawley rats were randomized to 13 groups (n=10/group), including nine groups in a three-by-three factorial design. Endpoints included P1NP, CTX-1, femoral bone mineral density measured by dual-energy X-ray absorptiometry (DXA), trabecular histology, and messenger ribonucleic acid and protein expression measured by reverse transcription quantitative polymerase chain reaction and Western blotting. The full formula (I2A2) was associated with higher P1NP, lower CTX-1, and higher BMD than the model group. Factorial analysis identified a Yin-Yang interaction between P1NP and BMD, supporting pharmacological synergy. Molecular changes were associated with increased EphB4/ephrinB2/ALP expression and reduced RhoA expression. These findings support an association between Zuogui Pill treatment, improved bone phenotypes, and modulation of pathway markers; causal pathway dependence requires inhibitor, knockdown, and co-culture validation. - Source: PubMed
Publication date: 2026/09/11
Dong ChongyangZhang XueliWang XiongyaoChen JianjunZhang ZengliangGao Xiaoming - Down-regulated -linked β--acetylglucosamine modification (-GlcNAcylation) has been implicated in Parkinson's disease (PD), and restoring -GlcNAcylation levels in the central nervous system via -GlcNAcase (OGA) suppression represents a potential therapeutic strategy for PD intervention. Nevertheless, naturally derived OGA inhibitors remain insufficiently explored, and the molecular mechanisms underlying OGA-inhibition-mediated restoration of -GlcNAcylation to alleviate PD remain poorly defined. Here, a fluorescence-based high-throughput inhibitor screening platform was established and subsequently used to identify sennoside A (SA) as a potent OGA inhibitor from an in-house phytochemical library. As a competitive OGA inhibitor, SA exhibited potent anti-OGA activity both in vitro and in vivo, along with favorable blood-brain barrier permeability and a well-tolerated safety profile. Moreover, SA markedly elevated protein -GlcNAcylation levels, which in turn attenuated neuroinflammatory response and ameliorated key PD-associated pathological and behavioral deficits. Mechanistically, SA directly inhibits OGA activity in neurons and microglia, predominantly enhancing the -GlcNAcylation of EphrinB2 at the Ser40/Thr183 sites and stabilizing EphrinB2. This site-specific modification activates the EphrinB2-EphB4 signaling cascade and subsequently blunts mitogen-activated protein kinase-mediated neuroinflammation. Disruption of EphrinB2 -GlcNAcylation by Ser40A/Thr183A mutation eliminates its neuroprotective function and abolishes the anti-PD effects of SA. Collectively, this work establishes the pharmacological inhibition of OGA as a promising therapeutic strategy for PD and identifies SA as a naturally occurring anti-PD agent that alleviates PD-associated pathological phenotypes by inhibiting OGA-mediated de--GlcNAcylation of EphrinB2. - Source: PubMed
Publication date: 2026/09/09
Wei GuilinJin ZhuoanMi HanyingLi NanWang WeiyuSong YunqingJin QiangGe GuangboLiu Yong - Male accessory sex glands are essential components of the reproductive system, providing secretions that support sperm function, fertility, and androgen-dependent reproductive processes. Despite the widespread use of mice as experimental models, comprehensive biometrical, histomorphometrical, and molecular characterization of their accessory sex glands remains limited. The present study investigated the vesicular, bulbourethral, and preputial glands of adult male mice with particular emphasis on biometric parameters, histological organization, and the expression of EphB2, EphB4, and ephrin-B1 membrane proteins. Ten-week-old male ICR mice ( = 6) were used for morphometric profiling, RT-PCR, and immunofluorescence analyses. The vesicular glands showed highly folded mucosa lined by pseudostratified columnar epithelial cells and enclosed by well-developed smooth muscle layers. Bulbourethral glands were multilobular, composed of arborized acini lined by tall columnar epithelial cells, whereas preputial glands were modified sebaceous glands characterized by lobulated sebaceous acini with prominent basal cells. RT-PCR analysis revealed the presence of EphB4 and ephrin-B1 transcripts in all three glands, while EphB2 expression was detected only in the vesicular and bulbourethral glands. Immunofluorescence staining demonstrated that EphB4 and ephrin-B1 were predominantly localized in basal cells of vesicular and preputial glands and in secretory epithelial cells in the bulbourethral gland, with weaker expression in principal cells in the vesicular gland. Faint expression of EphB2, EphB4, and ephrin-B1 was observed in α-SMA-positive smooth muscle cells of vesicular and bulbourethral glands. The findings provide the first integrated biometric and histomorphometric data and demonstrate distinct expression profiles of EphB2/B4 and ephrin-B1 membrane proteins in mouse accessory sex glands, suggesting their involvement in glandular structure and functional regulation. - Source: PubMed
Publication date: 2026/06/22
Gofur Md RoyhanToma Mst Suriya TanjumNakajima TakayukiTanida Takashi - 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