EPHB2 Control Peptide antibody /CP
- Known as:
- EPHB2 Control Peptide (anti-) /CP
- Catalog number:
- 'AM11064CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EPHB2 Control Peptide antibody /
Related genes to: EPHB2 Control Peptide antibody /CP
- 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 Control Peptide antibody /CP
Related articles to: EPHB2 Control Peptide antibody /CP
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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
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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 - Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype. - Source: PubMed
Publication date: 2026/04/16
Li GuoqiangJianhan FuGu JiashuWang YinhuaiLiu JiachenYang DongZeng DianjieZhao Pengcheng