EphB2, Active Human Recombinant Protein
- Known as:
- EphB2, Active Human Recombinant Protein
- Catalog number:
- 40200
- Product Quantity:
- 10 µg
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- EphB2 Active Human Recombinant Protein
Related genes to: EphB2, Active Human Recombinant Protein
- Gene:
- EPHB2 NIH gene
- Name:
- EPH receptor B2
- Previous symbol:
- DRT, ERK, EPHT3
- Synonyms:
- Hek5, Tyro5
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2019-04-23
Related products to: EphB2, Active Human Recombinant Protein
Related articles to: EphB2, Active Human Recombinant Protein
- Atherosclerosis (AS) is a major cause of cardiovascular diseases, with OX-LDL-induced VSMC dysfunction being a critical pathogenic driver of AS development. Saikosaponin D (SSD), a bioactive compound, shows therapeutic potential, but its mechanism in AS is unclear. - Source: PubMed
Yan MeihuaTang TianWang YanxiuQin YuzhenHao QiangweiChen XinriLuo Xianmin - Long noncoding RNAs (lncRNAs) have significant impacts on the occurrence and development of many cancers. However, their effects and mechanisms on prostate cancer (PCa) remain largely unknown. The study was to explore the influence of lncSPATA8-AS1 on PCa and its molecular mechanism of action. - Source: PubMed
Publication date: 2026/05/26
Zhong JinmanDeng YanmengQin XingruYang Quanxin - Vasculogenic mimicry (VM) and epithelial-mesenchymal transition (EMT) contribute to cervical cancer invasiveness and treatment resistance, yet the upstream regulators coordinating these plasticity programs remain incompletely defined. Ephrin receptor B2 (EPHB2) promotes malignant phenotypes in multiple tumor types; however, its functional role and mechanistic basis in cervical cancer, particularly in VM-associated plasticity, remain unclear. - Source: PubMed
Publication date: 2026/05/16
Jiao WenzhiLiu ShanshanHuai QingyangZhang ZiyueHe QinyuanYang XiaoqinYu Minmin - To evaluate the prognostic value of complement and coagulation cascades (CCC) in lung adenocarcinoma (LUAD). - Source: PubMed
Publication date: 2026/05/07
He BinbinZhu RangfeiLi NaLi Wei - 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