Ask about this productRelated genes to: EPHA4 antibody
- Gene:
- EPHA4 NIH gene
- Name:
- EPH receptor A4
- Previous symbol:
- TYRO1
- Synonyms:
- Hek8
- Chromosome:
- 2q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-02
- Date modifiied:
- 2016-10-05
Related products to: EPHA4 antibody
Related articles to: EPHA4 antibody
- Erythropoietin-producing hepatocellular carcinoma (Eph) receptor A4 (EphA4) binds to a broad range of ephrin ligands and is upregulated in various tumors. EphA4 activation plays crucial roles in the maintenance of cancer invasiveness, immune evasion, and stem cell properties. Furthermore, a novel EphA4 ligand, secretory ribonuclease 1, has been identified, and its interaction stimulates EphA4 signaling, leading to the promotion of cancer stem cell properties. Therefore, EphA4 has been considered an attractive target for cancer therapies. Thus, monoclonal antibodies (mAbs) against EphA4 are essential for basic research and mAb-based treatment in the clinic. In this study, we developed a novel anti-human EphA4 mAb, EaMab-3, using the Cell-Based Immunization and Screening (CBIS) method. EaMab-3 reacted with EphA4-overexpressed Chinese hamster ovary-K1 (CHO/EphA4) and endogenous EphA4-positive lung squamous cell carcinoma LK-2 in flow cytometry. The binding affinities (apparent dissociation constant values) were determined as 4.5 × 10 M for CHO/EphA4 and 2.5 × 10 M for LK-2. Furthermore, EaMab-3 did not exhibit cross-reactivity with other Eph receptor-overexpressed CHO-K1 cells. In addition, EaMab-3 is suitable for immunoblotting and immunohistochemistry. These results indicate that EaMab-3, established using the CBIS method, facilitates basic studies of EphA4 and is expected to be useful for mAb-based tumor diagnosis and therapy. - Source: PubMed
Publication date: 2026/05/23
Saga AyanoLi GuanjieTanaka TomohiroKaneko Mika KSuzuki HiroyukiKato Yukinari - The molecular and histologic characteristics associated with the development of post-traumatic capsular fibrosis of the shoulder joint following open reduction and internal fixation (ORIF) of proximal humerus fractures (PHF) remain incompletely understood. To help elucidate these mechanisms, this hypothesis-generating pilot study aimed to examine gene expression and histological changes in the joint capsule of patients undergoing implant removal and adhesiolysis for post-traumatic stiffness after surgical fixation of PHF. - Source: PubMed
Publication date: 2026/05/08
Henssler LeopoldDrenkard DanielaRiedl MoritzKlute LisaKeil FelixAlt VolkerRiool MartijnKerschbaum Maximilian - Blood-brain barrier (BBB) disruption is a key pathological event following traumatic brain injury (TBI), yet its molecular and spatial characteristics remain incompletely understood. Here, we developed a dual dye-labeling system to assess the temporal and spatial dynamics of BBB permeability following controlled cortical impact (CCI) injury in (KO) and (WT) mice. By tracking Evans Blue Dye (EBD), sodium fluorescein (NaFl), and IgG deposition, we reveal distinct patterns of extravasation in the injured cortex and hippocampus. NaFl, a small-molecule tracer, continues to extravasate for 7 days post-injury, whereas EBD leakage diminishes after 4 days. Notably, EC-specific EphA4 KO mice exhibit a protective role in BBB integrity. To further investigate BBB regulation, we integrated spatial transcriptomics with dye quantification, revealing that EphA4 EC ablation upregulates key BBB-related genes () and neuroprotective genes ( and ). Notably, Wnt signaling genes are upregulated in the KO cortex, and we demonstrate that inhibition of Frizzled-4 (FZD4)/Wnt attenuates BBB protection in KO mice. Importantly, direct pharmacological activation of Wnt signaling with the FZD4 agonist FZM1.8 reduces lesion volume and BBB disruption. Overall, these findings demonstrate the effectiveness of spatial transcriptomics and dual-dye labeling in uncovering region-specific transcriptional changes associated with BBB disruption following CCI injury and in assessing the influence of EphA4/Wnt signaling. Wnt signaling emerges as a promising pathway for BBB protection and repair following TBI, offering a potential strategy to mitigate secondary brain injury. - Source: PubMed
Publication date: 2026/04/09
de Jager CarolineJu JingCorbo MarcoPatel KaranTheus Michelle - Effective repair of peripheral nerve injuries often requires nerve grafts, yet outcomes remain suboptimal due to limited intrinsic regenerative support. Developing bioactive grafts to actively orchestrate the regenerative microenvironment is a critical unmet need. Our previous studies have demonstrated that extracellular vesicles from skin-derived precursor Schwann cells remarkedly enhance peripheral nerve regeneration. The purpose of this study was to investigate the molecular mechanisms by which extracellular vesicles from skin-derived precursor Schwann cells influence peripheral nerve regeneration. We established rat models of sciatic nerve defects and designated three intervention groups: autograft, nerve grafts incorporating extracellular vesicles from skin-derived precursor Schwann cells, and a control group with nerve grafts (silicone conduits filled with vehicle). Nerve injury was induced and surgical implantation of the respective grafts to bridge the defect was performed. Transcriptomic profiles (RNA-sequencing) and bioinformatic analyses were performed at 11 time points spanning the 12-week period post-injury. Weighted gene co-expression network analysis revealed that critical regenerative processes, including axon regeneration, myelination, angiogenesis, inflammatory chemotaxis, cell death, and proliferation/migration, occurred in distinct temporal phases. Notably, the nerve grafts incorporating extracellular vesicles from skin-derived precursor Schwann cells demonstrated more robust and temporally coordinated activation of these processes compared with the control groups. Importantly, we found that the nerve grafts incorporating extracellular vesicles from skin-derived precursor Schwann cells downregulated Epha4, which encodes Ephrin receptor A4, a transmembrane receptor known to inhibit Schwann cell migration and myelination. We further identified that vesicle-enriched miR-20b-5p directly targets Epha4. Functional assays confirmed that miR-20b-5p overexpression promoted Schwann cell migration and myelination, whereas its inhibition within nerve grafts incorporating extracellular vesicles from skin-derived precursor Schwann cells attenuated their pro-regenerative effects. This study provides a comprehensive temporal transcriptomic atlas of nerve regeneration and demonstrates that nerve grafts incorporating extracellular vesicles from skin-derived precursor Schwann cells modulate the regenerative microenvironment after peripheral nerve injury via the miR-20b-5p/Epha4 axis. These results offer critical mechanistic insights regarding nerve regeneration and novel therapeutic perspectives for extracellular vesicle-based neural repair strategies. - Source: PubMed
Publication date: 2026/04/14
Shen DingdingShi HaiyanYu YangCong MengZhang JunSong LiuchangZhou JiayiDing FeiLuo GuanghuaYu Miaomei - Colorectal cancer (CRC) typically follows the "normal-adenoma-carcinoma" (NAC) progression, with approximately 70-90% of cases driven by an adenomatous polyposis coli (APC) mutation-dependent pathway. The Apc-mutant (Min) mouse, valuable for dissecting gene function and mechanisms in CRC, provides an important basis for cross-species analyses with human data. Here, we performed a cross-species analysis of single-cell and spatial transcriptomic data across multiple stages of colorectal tissues in both humans and Min mice, constructing a spatiotemporal atlas. Our study identified key microenvironmental regulatory networks involved in CRC progression and highlighted the central role of epithelial-macrophage interactions within the tumor microenvironment. We further validated the suitability of the Min mouse as a model for the intrinsic Consensus Molecular Subtypes 2(iCMS2) microsatellite-stable (MSS) subtype of CRC. Focusing on the crosstalk between tumor-associated macrophages (TAMs) and epithelial cells, we identified the EFNA1-EPHA4 axis as a critical regulator promoting the immunosuppressive polarization of TAMs and enhancing tumor cell stemness. In addition, inhibition of EFNA1 was found to slow tumor growth. This study not only provides a systematic framework for mapping CRC correspondence between humans and mice, but also uncovers key molecular mechanisms underlying CRC progression and proposes promising therapeutic targets. - Source: PubMed
Publication date: 2026/04/09
Zhang SiwenXu KunDu YanyunLiu ZhenhaoLi HongLi BingXie LuZhong Yunshi