EphA4, affinity purified antiibody, goat, 100 ug.
- Known as:
- EphA4, antigenic enriched antiibody, caprine, 100 ug.
- Catalog number:
- GT15035-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- EphA4 affinity purified antiibody goat 100 .
Related genes to: EphA4, affinity purified antiibody, goat, 100 ug.
- 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, affinity purified antiibody, goat, 100 ug.
Related articles to: EphA4, affinity purified antiibody, goat, 100 ug.
- 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 - Ephrin (Eph) receptors play key regulatory roles in physiological processes, such as tissue development, cell migration, and angiogenesis. Upregulation of specific Eph receptors has been identified in many different cancers, highlighting Eph receptors as promising targets for new cancer therapeutics. Though targeting individual Eph receptors is challenging because of the high sequence homology among the 14 Eph receptors in humans, peptides have been isolated through phage display that target specific receptors (EphA2, EphA4, EphB2, EphB4). While many of these peptides have been further optimized based on the original phage display hits, the EphB2 receptor-targeting SNEW peptide has received less attention. Here we describe parallel strategies to modify SNEW, leading to improved affinity for the EphB2 receptor and greater stability in human serum while retaining SNEW's high specificity for the EphB2 receptor. Specifically, replacement of the N-terminal serine residue with cyclic α-amino acids, particularly those with saturated, six-membered rings, increased inhibitory potency against the EphB2 receptor-ephrin B2 interaction. Replacement of a central proline residue with 4,4-difluoroproline led to a significant increase in serum stability in the context of SNEW and its more potent N-terminally modified variants. SNEW variants with greater potency and serum stability offer lead candidates for targeting the EphB2 receptor in associated cancers and other diseases. Additionally, the modification approaches employed for SNEW may be extensible for N-terminal serine/threonine/cysteine substitution and/or proline substitution to improve protein targeting by other peptides. - Source: PubMed
Publication date: 2026/04/03
Garcia Brian EEpstein Sophie RLegarreta Sofia ATennett Jessica CCain Jenna MSawyer Nicholas - Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies with a 5-year survival rate of approximately 12%. Treatment options, including surgical resection and chemotherapy, are often ineffective in advanced stages due to late detection. This review examines the role of Erythropoietin-producing human hepatocellular (Eph) receptors in PDAC, emphasizing their potential both as therapeutic targets and biomarkers. Eph receptors, a family of receptor tyrosine kinases, are frequently overexpressed in various cancers and contribute to tumor growth, angiogenesis, and metastasis. Among the molecular drivers implicated in PDAC, EphA2, EphA4, EphA10, and EphB4, have emerged as key players in tumor progression, metastasis, resistance to therapy and poor prognosis. Eph receptor fragments show potential as early detection and prognostic biomarkers, potentially offering higher sensitivity than traditional markers such as CA 19-9. Additionally, emerging therapies targeting these receptors, such as EphA2-directed drug conjugates and small-molecule inhibitors, show promising results in preclinical models. Despite these advancements, their clinical translation remains limited, because of low specificity, poor delivery, and lack of validation in large patient cohorts. This review underscores the significance of Eph receptors in PDAC biology and highlights their dual utility as biomarkers and therapeutic targets, emphasizing the need for in depth investigation to bridge the gap between experimental promise and clinical reality. Harnessing Eph receptor biology holds the potential to improve early diagnosis and open new avenues for precision therapy and better treatment outcomes in one of the deadliest cancers. - Source: PubMed
Publication date: 2026/03/26
van de Langerijt Karlijn AWestveen JaneKazemier GeertPeters Godefridus Jle Large Tessa Y SGiovannetti Elisa