Anti-Mouse CD309 (FLK1) PE 200 ug
- Known as:
- Antibody toMouse CD309 (FLK1) PE 200 ug
- Catalog number:
- 12-5821-83
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD309 (FLK1) 200
Related genes to: Anti-Mouse CD309 (FLK1) PE 200 ug
- Gene:
- KDR NIH gene
- Name:
- kinase insert domain receptor
- Previous symbol:
- -
- Synonyms:
- FLK1, VEGFR, VEGFR2, CD309
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD309 (FLK1) PE 200 ug
Related articles to: Anti-Mouse CD309 (FLK1) PE 200 ug
- 6PPD and its ozonation product 6PPD-quinone (6PPD-Q) are widespread tire-derived pollutants. This study combined network toxicology, clinical transcriptomics, molecular docking, and experimental validation to investigate their intestinal toxicity mechanisms and potential molecular relevance to inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Database screening identified 213 predicted targets for 6PPD and 165 for 6PPD-Q. Venn analysis identified 160 and 61 targets shared between 6PPD and CD- and UC-associated genes, respectively, whereas 112 and 105 targets were shared between 6PPD-Q and CD- and UC-associated genes, respectively. Network analyses showed that 6PPD-associated targets were mainly enriched in inflammatory signaling and oxidative stress-related pathways involving candidate hubs such as HIF1A, IL1B, IL6, and PTGS2. In comparison, 6PPD-Q-associated targets were enriched in kinase-signaling and mucosal-repair-related pathways involving HCK, KDR, LYN, EGFR, and MAPK14. Molecular docking predicted favorable binding poses between the compounds and the selected candidate targets, with docking scores ranging from -6.0 to -8.8 kcal/mol. Comparisons with clinical transcriptomic datasets further showed that several candidate targets were dysregulated in inflamed IBD tissues. In vivo, repeated exposure of C57BL/6 mice to 6PPD or 6PPD-Q for 40 days resulted in colon injury, reduced expression of intestinal tight-junction proteins, and increased expression of inflammatory mediators. In RAW264.7 macrophages, both compounds induced dose-dependent cytotoxicity, ROS production, and increased proinflammatory gene expression. These findings demonstrate that 6PPD and 6PPD-Q induce intestinal injury, oxidative stress, and inflammatory activation in experimental models and affect molecular targets and pathways implicated in IBD. Further studies using established experimental IBD models are warranted to determine whether these compounds exacerbate pre-existing intestinal inflammation or influence disease severity. - Source: PubMed
Publication date: 2026/08/22
Zhang YixuanLuo YuyangWang SiyiLi Ze - Thin endometrium (TE) is an important factor associated with embryo implantation failure and adverse pregnancy outcomes during assisted reproductive treatment. This study investigated the clinical efficacy of fixed-dose motherwort injection (MI) combined with different doses of compound estradiol/dydrogesterone tablets (CPET) in the treatment of TE, evaluated its effects on endometrial receptivity, and determined the optimal therapeutic dose of CPET. - Source: PubMed
Publication date: 2026/07/15
Wang TangxiaomanWei FangJiang JialiHe Jing - Angiogenesis plays a crucial role in tumor growth, progression, and metastasis, making the vascular endothelial growth factor receptor-2 (VEGFR2) a key therapeutic target in anticancer drug development. In this study, an integrated in silico and in vitro strategy was applied to identify novel potential inhibitors of VEGFR2. Initially, a dataset of VEGFR2 inhibitors with reported biological activities was collected from the ChEMBL database. Pharmacophore models were generated using a ligand-based approach, and the most relevant hypotheses were selected to construct three-dimensional quantitative structure-activity relationship (3D-QSAR) models. Subsequently, a virtual screening workflow including pharmacophore mapping, QSAR modeling, and molecular docking using the VEGFR2 crystal structure (PDB ID: 3WZD), followed by Absorption, Distribution, Metabolism, Excretion, and Toxicity (ADMET) filtering, was performed to identify the most promising hits. Based on the computational screening results, ten compounds were purchased and experimentally evaluated for their antiproliferative activity using the MTT cytotoxicity assay on three human cancer cell lines known to express VEGFR2: MCF-7 and MDA-MB-231 (breast cancer) and HepG2 (hepatocellular carcinoma). Four hits exhibited moderate antiproliferative activity against HepG2 cells (IC = 28.6-90.5 µM), while no significant activity was observed against the breast cancer cell lines MCF-7 and MDA-MB-231. Overall, this study identifies several structurally novel compounds as promising potential VEGFR2 inhibitors and supports the effectiveness of integrating pharmacophore modeling, QSAR analysis, molecular docking, and experimental validation for anticancer drug discovery. - Source: PubMed
Publication date: 2026/08/22
Meziani OuafaAit Kaki SamiraFerkous FouadKraim KhairedineLayachi FaycalSaihi YoucefKüçükkılınç Tuba TüylüTürk Seyhan - Cardiovascular-kidney-metabolic (CKM) syndrome confers elevated mortality risk, but whether dietary ketogenic ratio (KDR) is associated with mortality in this population remains unclear. We examined the association of KDR with mortality in adults with CKM syndrome and whether it persisted after accounting for broader diet-quality metrics. - Source: PubMed
Publication date: 2026/08/05
Guo HuiWang LeiXiao Fangping - Oral squamous cell carcinoma (OSCC) is an aggressive malignancy with poor clinical outcomes driven by metastasis and recurrence. Vascular endothelial growth factor receptor 2 (VEGFR2), a key mediator of VEGFA-dependent angiogenesis, has recently been implicated in tumor cell-intrinsic signaling; however, its role in OSCC remains unclear. This study investigated VEGFA-VEGFR2 signaling in OSCC using a 4-nitroquinoline 1-oxide (4NQO)-induced mouse carcinogenesis model and human tissue specimens. Spatial transcriptomic analysis of murine tongues demonstrated enrichment of Kdr (Vegfr2) and Vegfa expression in tumor regions. Immunohistochemical analyses demonstrated upregulation of VEGFR2, particularly nuclear VEGFR2, during tumor development. Exogenous VEGFA increased VEGFR2 expression and induced its nuclear localization in murine carcinoma cells. In human tongue squamous cell carcinoma (TSCC), VEGFR2 was localized in the cytoplasm and nucleus, and nuclear VEGFR2 expression was significantly associated with tumor stage, lymph node metastasis, and proliferative activity. Nuclear VEGFR2 expression also correlated with VEGFA expression in epithelial and stromal compartments. Functional analyses showed that VEGFA-VEGFR2 signaling enhanced cell migration and stem-like properties independently of angiogenesis. These findings indicate that nuclear VEGFR2 reflects pathway activation and contributes to tumor aggressiveness, highlighting its potential as a biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/08/19
Li Li-JieTeramoto AkariUsami YuHirose KatsutoshiHata KenjiChang Wei-MinFeng Sheng-WeiToyosawa Satoru