EPHB3 Clone '50CT97.1.9 antibody Host
- Known as:
- EPHB3 Clone '50CT97.1.9 (anti-) Host
- Catalog number:
- 'AM11065SU-N
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EPHB3 Clone '50CT97.1.9 antibody Host
Related genes to: EPHB3 Clone '50CT97.1.9 antibody Host
- 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 Clone '50CT97.1.9 antibody Host
Related articles to: EPHB3 Clone '50CT97.1.9 antibody Host
- The greatest cause of death from breast cancer is metastasis, yet little is known about the molecular mechanisms behind this phenomenon. Using four publically accessible datasets, we conducted a thorough transcriptome analysis of 187 samples from seven breast cancer metastatic sites: the brain, bone, lung, liver, lymph nodes, skin, and local-regional skin (skinlr). Of the 12,005 genes that were found to be shared by all samples in this investigation, 604-885 differentially expressed genes (DEGs) were unique to each metastatic location. Pathways including PI3K-Akt signaling, prolactin signaling, complement, and coagulation cascades were identified by functional enrichment analysis as important metastasis drivers with unique functions in different locales. The results of regulatory analysis revealed 77 upstream factors, including 14 kinases (like EPHB3, PAK3) and 63 transcription factors (like ESR1, FOXA1, and GATA3), some of which were discovered for the first time in breast cancer metastases (like TCF4, HOXA10). It was shown that hub genes including MMP9, SPP1, and PDGFRB are essential for the survival and development of metastases, offering new information on site-specific biology. Crucially, by identifying site-specific molecular markers, these discoveries pave the way for personalized medicine techniques and allow tumor-specific therapy tactics, such as targeting Central Carbon Metabolism in lung and skin metastases. This work provides actionable options for tumor-specific treatment and tailored interventions by highlighting new molecular candidates and signaling pathways for metastatic breast cancer. - Source: PubMed
Publication date: 2026/05/12
Salari AliMikaeili Namini ArshamAlipour AramFarahani FatemehSalehi FarnazShafiei Tehrani Zahra SadatBagherpour GhasemYosefy FatemehJafari DelaramShahbazi AliMirzaei Chegeni MasoumehKhodadad Hossyni Mohammad AminSafari Kharkheshi MahboubehBakhshi Manjili Monire - 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
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