Anti_Mouse, mab EphA4 Source Rat
- Known as:
- Anti_Mouse, mab EphA4 Source Rat
- Catalog number:
- 103-M166
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab EphA4 Source Rat
Related genes to: Anti_Mouse, mab EphA4 Source Rat
- 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: Anti_Mouse, mab EphA4 Source Rat
Related articles to: Anti_Mouse, mab EphA4 Source Rat
- Sevoflurane may induce neurotoxicity and cognitive impairment, though the associated mechanisms remain unclear. This study aimed to investigate how long non-coding RNA CEBPA-AS1 contributed to the neurotoxicity and cognitive impairment induced by sevoflurane. This study employed HT22 hippocampal neuronal cells and 18-month-old Sprague-Dawley rats to establish a sevoflurane exposure model. Reverse transcription quantitative real‑time polymerase chain reaction (RT‑qPCR) was employed to detect relevant gene expression. Cell proliferation, apoptosis, inflammatory levels, and oxidative stress indicators were assessed using cell counting kit‑8 (CCK‑8) assays, flow cytometry, enzyme‑linked immunosorbent assay (ELISA), and oxidative stress kits. The Morris water maze was used to evaluate rats' learning and memory abilities. The RNA immunoprecipitation (RIP) assay and dual luciferase assay were utilised to validate the targeted binding relationship of the target molecules. Sevoflurane treatment significantly increased CEBPA-AS1 expression in HT22 cells and rat hippocampal tissue while simultaneously downregulating microRNA-455-3p (miR-455-3p) and upregulating erythropoietin-producing hepatocellular carcinoma A4 (EPHA4). Silencing CEBPA-AS1 significantly alleviated sevoflurane-induced cellular and brain tissue injury, apoptosis, oxidative stress, and inflammatory responses, whilst concurrently improving cognitive impairment at the in vivo level. Mechanistic studies showed CEBPA-AS1 acted as a molecular sponge for miR-455-3p, which targeted and repressed EPHA4, thus forming the CEBPA-AS1/miR-455-3p/EPHA4 regulatory axis. Rescue experiments showed that miR-455-3p inhibition partially reversed the attenuation of sevoflurane neurotoxicity by CEBPA-AS1 silencing, restoring neurotoxicity, oxidative stress, inflammation, and cognitive impairment in vitro and in vivo. On this basis, EPHA4 inhibition blocked the competitive endogenous RNA (ceRNA) axis-mediated toxic effects, relieving these neurotoxic phenotypes and cognitive dysfunction again. The CEBPA-AS1/miR-455-3p/EPHA4 axis mediated sevoflurane-induced neurotoxicity and subsequent cognitive impairment. - Source: PubMed
Fu JinpengYuan Ya-WeiMa Zhen - MicroRNAs (miRNAs) attract attention in depression and related cognitive impairment research, with genetic factors in their regulation of depressive emotions and cognition growing prominent. The genetic association between the rs4705342 polymorphism and susceptibility to cognitive impairment in depressive adolescents was explored, along with its underlying mechanism. - Source: PubMed
Publication date: 2026/06/27
Zhu JunjuanZhang DongziLi Jing - Precise measurements of small molecule-protein interactions are critical for drug discovery. However, most biochemical profiling platforms measure binding using recombinant kinase domains or proteins in cell lysates, which can miss conformational regulation present in intact living cells. Here, we used flow cytometry-based fluorescent probe cellular binding assays (FPCBA) to demonstrate that the anticancer drug dasatinib binds native, untagged ABL1 kinase with 3-6-fold higher affinity than NanoLuc- or mVenus-tagged constructs in living cells. We further used this method for in-cell profiling of 25 native kinases, revealing conformational regulatory mechanisms, including SRC autoinhibition and membrane-dependent conformational states of DDR1, DDR2, and EPHA4 that are absent or attenuated in biochemical assays. For these studies, coumarin-dasatinib probes spanning a range of fluorophore acidity (p 4.1-7.3) were optimized for intracellular target engagement. To enhance sensitivity of detection, we found that uptake of acidic probes can be promoted by expression of the organic anion transporter OATP1B3. Quantitative flow cytometry with NIST-standardized beads established that intracellular concentrations of an intermediate-acidity 6FC-dasatinib probe approximated extracellular concentrations in HEK293T cells at equilibrium. Cellular values of dasatinib and imatinib for 25 kinases by FPCBA were broadly concordant with kinobead LC/MS measurements in cancer cell lysates but diverged substantially from recombinant KINOMEscan values, with divergences attributable to competition with ATP, autoinhibition, and membrane-dependent conformational states in living cells. FPCBA enables profiling of native protein-small molecule interactions in a physiologically relevant cellular context. - Source: PubMed
Publication date: 2026/06/23
Cool Lillian MPawar JogendraSonam SonamKumari SmitaZhao Serena LiHu XiaojunLin ZhihongWu MengHu ShuiyingPeterson Blake R - - Source: PubMed
Publication date: 2026/06/12
Zhang SiwenXu KunDu YanyunLiu ZhenhaoLi HongLi BingXie LuZhong Yunshi - STXBP1 haploinsufficiency, a major genetic cause of developmental and epileptic encephalopathies, exhibits variability in clinical severity and remains poorly understood mechanistically. Although STXBP1 encodes a core presynaptic protein essential for SNARE-mediated neurotransmitter release, evidence from rodent models and patient-derived neurons indicates that its deficiency produces far broader molecular and cellular disruptions across multiple neurodevelopmental processes. Understanding how these widespread perturbations contribute to STXBP1 encephalopathy requires integrative approaches that extend beyond single-phenotype assays. Here, we used foetal human organotypic cortical cultures that preserve tissue architecture including the transient subplate, a critical hub in early cortical network development. Human cultures (15-18 post-conception weeks) retaining intact subplate, cortical plate, and progenitor zone organisation, were subjected to shRNA-mediated STXBP1 knockdown. We combined live calcium imaging, targeted transcriptomics, protein expression validation, and neurite-growth assays to assess functional and structural outcomes. STXBP1 knockdown disrupted spontaneous subplate neuronal network activity observed by calcium imaging at 14 days in vitro, reducing signal amplitude and synchronicity, indicating impaired early circuit function. Transcriptomic profiling revealed dysregulation of gene expression involved in synaptogenesis, ion transport, and extracellular matrix organisation. Protein-level analyses confirmed alterations in key synaptic components. At the cellular level, neurons exhibited shortened neurites and accumulation of the axon-guidance receptor EPHA4 at growth cones, suggesting defects in early connectivity. These findings expand the mechanistic framework of STXBP1 encephalopathy beyond synaptic dysfunction to encompass coordinated molecular, structural and network-level pathology during a critical window of cortical development, highlighting convergent pathways that may inform early therapeutic strategies. - Source: PubMed
Publication date: 2026/05/28
McLeod FayeDimtsi AnnaSavage Michael ATan Yen ChiHedley AnnTrevelyan Andrew JClowry Gavin J