Ask about this productRelated genes to: EphB3 antibody
- Gene:
- EPHB3 NIH gene
- Name:
- EPH receptor B3
- Previous symbol:
- ETK2
- Synonyms:
- Hek2, Tyro6
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-07
- Date modifiied:
- 2015-09-11
Related products to: EphB3 antibody
Related articles to: EphB3 antibody
- Neuropathic pain after spinal cord injury reflects persistent hyperexcitability in the spinal cord dorsal horn, yet the molecular drivers sustaining this maladaptive state are unknown. Using an antibody microarray of dorsal horn tissue from mice six weeks after cervical contusion spinal cord injury, we found persistent upregulation of Eph-ephrin signaling, including increased EphB1, EphB2 and EphB3 expression and phosphorylation. Reversible chemogenetic inhibition of EphB kinase activity, using an EphB1/2/3 analog-sensitive knock-in mouse, selectively reversed established mechanical allodynia without affecting thermal hyperalgesia or motor function and also shifted dorsal horn signaling away from pain sensitization-associated pathways. Among EphB receptors, EphB2 showed the most consistent and robust injury-induced increase in expression within dorsal horn. Although EphB2 transcript levels increased in both dorsal horn neurons and astrocytes, conditional deletion of EphB2 only in dorsal horn neurons, but not in astrocytes, reversed established mechanical allodynia and reduced dorsal horn neuronal activation. These findings identify EphB signaling, and neuronal EphB2 in particular, as a mechanism that actively maintains pain hypersensitivity after spinal cord injury. - Source: PubMed
Publication date: 2026/04/22
Heinsinger Nicolette MJaffe David ASrikanth Kolluru DLyttle Megan ASmith Madison SThomas Samantha JCharsar Brittany ACheng LanMichel-Flutot PaulineCain Rachel EWatson Jaime LBao DuranFan JiaFalnikar AditiZhou WeiDalva Matthew BLepore Angelo C - Traumatic brain injury (TBI) is among the most devastating condition and involves primary and secondary injury cascades. The blood-brain barrier (BBB) is a selective, semipermeable membrane that tightly controls the brain's microenvironment for proper neuronal function. Existing evidence demonstrates that TBI impairs the integrity and function of the BBB, leading to not only acute pathological changes but also long-term neuropathological consequences. Multiple BBB-related signaling molecules (e.g., Tie-2, EphB3, and Cav-1) are involved in the pathophysiological processes post-injury. These can result in microcirculatory insufficiency, neurotoxin accumulation, and cerebral edema after TBI. Together, such events synergistically cause axonal damage, neuronal cell death, and neuroinflammatory responses, which underlie the pathogenesis of TBI. In this review, we aim to summarize the pathophysiological roles of BBB breakdown in TBI, survey underlying mechanisms, and discuss therapeutic potential for this notorious disease by regulating the BBB. - Source: PubMed
Publication date: 2026/04/11
Wu HaijianZheng JingweiXu WeilinZhou FengqiLenahan CameronGiamas GeorgiosWang ChunZhang JianminJi Jianxiong - Triple-negative breast cancer (TNBC) is an aggressive subtype lacking estrogen and progesterone receptors and HER2 amplification. Representing 10-15% of breast cancer cases, TNBC disproportionately affects Black and pre-menopausal women and is associated with poorer outcomes. With chemotherapy as the primary systemic treatment option, achieving a pathological complete response (pCR) to neoadjuvant chemotherapy (NAC) is a key prognostic factor. However, TNBC biological heterogeneity complicates treatment response prediction. This study aimed to identify transcriptomic biomarkers predictive of NAC response in TNBC patients and evaluate machine-learning models for response classification. - Source: PubMed
Publication date: 2026/03/26
Amniouel SoukainaJafri Mohsin Saleet - Breast cancer (BC)-related atrial fibrillation (AF) contributes to an overall poor prognosis and raises great concerns. However, beyond cancer treatment-related AF, it is unknown whether BC itself is sufficient to directly induce AF. This study aimed to explore the role of BC in the development of AF, focusing on the tumour itself rather than therapy-related cardiotoxicity. - Source: PubMed
Publication date: 2026/03/05
Xue GenlongZhang PuyuZhan GeWang XinDong HaoyuLiu FeiCai ZhengangLi XinyiNa YuxinWen YuhangHan XuXu RongqianYang YihengPeng YiweiWang ShihaoWang HongjiangChe YingZhang YanXia YunlongPan ZhenweiYang Xiaolei - Ephrin type-B receptor 3 (EphB3) binds to transmembrane ephrin-B ligands to regulate cell migration, adhesion, and proliferation. EphB3 exhibits a gradient expression pattern in the normal intestine, with the highest levels at the crypt base, and plays a crucial role in the maintenance of normal intestinal epithelium. Therefore, anti-EphB3 monoclonal antibodies (mAbs) are required for basic research and diagnosis. In this study, we developed novel antihuman EphB3, EbMab-5 (IgG, κ) and EbMab-11 (IgG, κ), using the Cell-Based Immunization and Screening (CBIS) method. EbMab-5 and EbMab-11 reacted with EphB3-overexpressed Chinese hamster ovary-K1 (CHO/EphB3) and endogenous EphB3-positive colorectal cancer LS174T in flow cytometry. The apparent binding affinity of EbMab-5 for CHO/EphB3 and LS174T was 7.6 × 10 M and 1.7 × 10 M, respectively. EbMab-11 could detect EphB3 in western blot analysis and immunohistochemistry. EbMab-5 and EbMab-11, established by the CBIS method, may contribute to the diagnosis and therapy of EphB3-positive tumors. - Source: PubMed
Publication date: 2026/01/28
Li GuanjieSuzuki HiroyukiKaneko Mika KKato Yukinari