Anti_Mouse, mab EphA7 Source Rat
- Known as:
- Anti_Mouse, mab EphA7 Source Rat
- Catalog number:
- 103-M170
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab EphA7 Source Rat
Related genes to: Anti_Mouse, mab EphA7 Source Rat
- Gene:
- EPHA7 NIH gene
- Name:
- EPH receptor A7
- Previous symbol:
- -
- Synonyms:
- Hek11
- Chromosome:
- 6q16.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-10
- Date modifiied:
- 2016-10-05
Related products to: Anti_Mouse, mab EphA7 Source Rat
Related articles to: Anti_Mouse, mab EphA7 Source Rat
- The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - Although human papillomavirus (HPV) testing and Thin-Prep Cytology Test (TCT) are currently adopted as the first-line screening methods for cervical cancer, both of them have limitations. This study aimed to develop and validate new methylation-based biomarkers from formalin-fixed paraffin-embedded (FFPE) tissue and TCT samples in a Chinese population to improve early detection of cervical cancer (CC). - Source: PubMed
Publication date: 2026/05/21
Liu ZhihanLiu GuorongLiu ShuanpingWang XiuxiuLiang YunshiGuo YuanyuanDu BaochenMiao NaboShi WenliZhu QiuyunYu LipingDeng CuiChen GuoHuang LijuanZhan LinglingZheng XiangyuZhao JieLi YongjunHan XiaoliangCheng YangYang Jing - Human papillomavirus (HPV) gene transcription activity and methylation could be promising tools for cervical cancer (CC) screening. This study compared HPV E6/E7 messenger RNA (mRNA) + ThinPrep cytology test (TCT) vs. HPV genotyping + TCT in screening CC and explored the relationship between gene methylation and cervical lesions. - Source: PubMed
Publication date: 2026/04/22
Zhao XinlingChang LeiDuan WenyanLiu LijuanShi YangeFan XiaolingBai YuWang YanliLi Jingya - Polycystic ovary syndrome (PCOS), a highly prevalent endocrine disorder in women of reproductive age, is strongly associated with infertility. This study explored the relevance of the regulation of KGN cell function by miR-196a-5p and the pathogenesis of PCOS. This study selected 105 patients with non-obese, hyperandrogenic PCOS and 88 healthy individuals as research subjects. The levels of miR-196a-5p and EPHA7 in cells were assayed by RT-qPCR. Diagnostic accuracy of miR-196a-5p for PCOS was analyzed by ROC curve and multivariate logistic regression analysis. Chi-square test was used to analyze the correlation between the differential expression of miR-196a-5p and clinical indicators. Cell proliferation and apoptosis were assayed by CCK8 and flow cytometry. Western blot was used to detect the expression of apoptosis-related proteins and EPHA7 protein. Relationship between EPHA7 and miR-196a-5p was detected through miRDB database and dual-luciferase reporter assay. Correlation between miR-196a-5p and EPHA7 in non-obese, hyperandrogenic PCOS patients was analyzed by Pearson correlation. In GCs from non-obese, hyperandrogenic PCOS patients, an up-regulation of miR-196a-5p levels was observed, while EPHA7 showed a down-regulation trend. ROC analysis showed that miR-196a-5p had a high diagnostic value for non-obese, hyperandrogenic PCOS patients. miR-196a-5p may be an independent risk factor for PCOS, and it is significantly positively correlated with clinical indicators. Overexpression of miR-196a-5p in KGN cells enhanced cell proliferation and reduced apoptosis, while inhibition of this miRNA expression reversed this effect. In PCOS, miR-196a-5p was negatively correlated with EPHA7. Furthermore, reducing EPHA7 levels counteracted the regulatory effects of miR-196a-5p downregulation on KGN cells. miR-196a-5p was upregulated in GCs from non-obese, hyperandrogenic PCOS patients and promoted cell proliferation and inhibited apoptosis by regulating EPHA7. Therefore, miR-196a-5p shows promise as a novel biomarker and therapeutic target for this subtype of PCOS. - Source: PubMed
Publication date: 2026/04/22
Wang QihangGu TeLing LiliZhang LiqinCao Bo - BACKGROUND: Pediatric acute myeloid leukemia (AML) is a biologically distinct and aggressive malignancy with limited effective therapies. While emerging targeted agents, including menin, FLT3, and PRMT5 inhibitors, show promise, the transcriptomic effects and the role of extracellular matrix (ECM) regulators, such as nidogen-1 (NID1), in modulating therapeutic responses remain unclear. METHODS: We performed integrative transcriptome analyses of pediatric AML datasets (TARGET-AML, GSE246783: MI3454; GSE292324: PRMT5 inhibition; GSE292050: NID1 knockdown) and incorporated adult AML data from TCGA and GTEx. Differential expression was evaluated using DESeq2 and limma, functional enrichment using ClusterProfiler, Metascape, and GSEA, and protein–protein interaction networks using STRING, Cytoscape, NetworkAnalyst, and GeneMANIA. Transcription factor (TF) and upstream regulator inference were conducted using DoRothEA/decoupleR, Enrichr, and TRRUST v2. RESULTS: MI3454 treatment altered 166 genes, including upregulation of MMP10, ABCB5, and RND3, and downregulation of CD38 and ANGPT1, indicating ECM remodeling and immunomodulation. PRMT5 inhibition affected 22 RNA-processing genes, while NID1 knockdown influenced 36 ECM-related genes. GSEA consistently highlighted ECM/MMP pathway enrichment. PPI analysis identified FN1, MMP10, and EPHA7 as central hubs. TF and upstream regulator analyses revealed a shared NF-κB, CEBPB, SP1, and STAT3 axis connecting MI3454 response, PRMT5 inhibition, and NID1 disruption. Compared to prior pediatric and adult AML transcriptomic studies, this work provides novel mechanistic insights into ECM remodeling as a central mediator of therapy response. CONCLUSIONS: Targeted therapies in pediatric AML converge on ECM remodeling and a shared TF-driven regulatory axis, highlighting combinatorial strategies targeting microenvironmental and signaling vulnerabilities to overcome treatment resistance. - Source: PubMed
Publication date: 2026/02/21
Daniel Muteb MuyeyAndwey Gradel Holel