VEGFR2 (Phospho_Tyr951) Antibody
- Known as:
- VEGFR2 (Phospho_Tyr951) Antibody
- Catalog number:
- E011086-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- VEGFR2 (Phospho_Tyr951) Antibody
Related genes to: VEGFR2 (Phospho_Tyr951) Antibody
- 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: VEGFR2 (Phospho_Tyr951) Antibody
Related articles to: VEGFR2 (Phospho_Tyr951) Antibody
- Epithelial ovarian cancer (EOC) is the deadliest gynecological malignancy. Ferroptosis, an iron-dependent lipid peroxidation-associated cell death mode, provides a new target for tumor therapy. Nevertheless, its impact on EOC tumorigenesis is not well defined. The quality control, dimensionality reduction, and EOC clustering for the gene expression data were performed through the Scanpy pipeline for single-cell RNA sequence from GEO (GSE165897). Ferroptosis pathway scoring, computation of transcription factor activity, and analyzes for cell-cell communication were conducted. An independent validation cohort (GSE300897, n = 19,002 cells) was analyzed to confirm ferroptosis signature robustness. Expression of ferroptosis-related genes in SKOV3 and OVCAR3 cells was confirmed using RT-qPCR and immunoassays after treatment with erastin, RSL3, and ferrostatin-1 rescue. NRF2 siRNA knockdown and co-culture experiments were performed for functional validation. A total of 51,702 cells from 11 patients were analyzed and clustered into 18 clusters that included EOC cells (16.9%), immune cells (67.6%), and stromal cells (15.6%), encompassing 27 fine-grained cell subtypes. KEGG enrichment revealed that ferroptosis, fatty acid metabolism, and glutathione metabolism were the major pathways. Transcription factor profiling indicated increased NRF2 activation in EOC cells, which implied an augmented ferroptosis-resistance capacity. Signaling between cells also revealed three key ligand-receptor interactions, SPP1-CD44, VEGFA-KDR, and CCL2-CCR2, which are involved in the regulation of ferroptosis and were functionally validated in a triple co-culture model. NRF2 siRNA knockdown synergistically enhanced erastin-induced ferroptosis sensitization (C11-BODIPY: 4.52-fold), rescued by ferrostatin-1. Platinum-refractory patients in GSE300897 showed significantly altered ferroptosis scores (Mann-Whitney p = 3.22e-24), linking ferroptosis to clinical platinum sensitivity. Our work uncovers ferroptosis dysregulation as a key driver of EOC pathogenesis, with NRF2 being a master regulator of resistance to ferroptosis and suggesting new therapeutic approaches for ovarian cancer. - Source: PubMed
Liu JieLi JingLi BingxinLiang Hui - Xiaotansanjiefang, a traditional Chinese medicine formula containing pinellia rhizomes, is investigated for anti-gastric cancer (GC) activity. Cycloartenol, a triterpenoid saponin from pinellia, exhibits emerging anti-tumor properties. This study evaluates its effects on GC cell migration, invasion, and angiogenesis. Cytotoxicity of cycloartenol (0-160 μM) was assessed in GC cells (AGS and MKN-45) and immortalized normal gastric epithelial cells (GES-1) via MTT assays. Colony formation, wound healing, and Transwell assays were conducted to assess proliferation, migration, and invasion. Angiogenesis was evaluated by HUVEC tube formation using conditioned media harvested from cycloartenol-treated GC cells. VEGFA and VEGFR2 protein levels were measured by Western blotting. Cycloartenol showed dose-dependent cytotoxicity in GC cells with minimal toxicity toward GES-1 cells, indicating selectivity. It suppressed colony formation, delayed wound closure, reduced invading cells, and inhibited HUVEC tube formation. Consistently, cycloartenol downregulated VEGFA and VEGFR2 expression in GC cells and HUVECs. In conclusion, cycloartenol selectively suppresses GC cell growth, migration, invasion, and angiogenesis through inactivation of the VEGFA/VEGFR2 pathway. - Source: PubMed
Chang ChengHuang GengFang Zheng - A new series of chromene derivatives (12-19) was rationally designed as potential inhibitors of vascular endothelial growth factor receptor-2 (VEGFR-2) by integrating essential pharmacophoric and structural features. The target compounds were synthesized and structurally confirmed using spectroscopic techniques. Their in vitro antiproliferative activities were evaluated against a panel of human cancer cell lines (MCF-7, MDA-MB-231, HepG-2, and HCT-116) alongside normal human cells (WI-38 and WISH), in addition to a VEGFR-2 enzyme inhibition assay. Among the synthesized derivatives, compound 17 emerged as the most potent candidate, displaying low micromolar IC values across all tested cancer cell lines and superior VEGFR-2 inhibitory activity (IC = 0.518 µM) compared with the reference drug sorafenib (IC = 0.809 µM). Mechanistic investigations revealed that compound 17 induced pronounced cell cycle arrest and triggered apoptosis, as demonstrated by Annexin V-FITC/PI flow cytometric analysis. Computationally, Density Functional Theory (DFT) calculations demonstrated favorable electronic properties for compound 17, supporting effective ligand-receptor interactions. Molecular docking and 100-ns molecular dynamics (MD) simulations, complemented by MM-GBSA binding free energy calculations, Protein-Ligand Interaction Fingerprinting (Pro-LIF), Principal Component Analysis (PCA-T), and Free Energy Landscape (FEL) analyses, confirmed the stability and favorable binding energetics of compound 17 within the VEGFR-2 active site. Furthermore, in silico ADME-Tox profiling predicted acceptable pharmacokinetic behavior and a favorable safety profile. Collectively, these experimental and computational findings identify compound 17 as a promising and mechanistically well-characterized VEGFR-2 inhibitor, warranting further in vivo investigation. - Source: PubMed
Elkady HazemAlsfouk Aisha AElkaeed Eslam BElgammal Walid EMahdy Hazem ANofal AhmedEissa Ibrahim HHusein Dalal ZAmin Fatma GMetwaly Ahmed M - Aedes aegypti is the primary vector of arboviruses such as dengue, yellow fever, Zika, and chikungunya. Here, we investigate the mitochondrial DNA (mtDNA) structure and insecticide resistance of Ae. aegypti populations across Kenya. Using 175 newly sequenced Kenyan COI mtDNA fragments, along with global reference sequences, we assess maternal ancestry and phylogeographic structure. Genetic structure across Kenya was not well explained by isolation-by-distance alone, with several populations deviating from this pattern. Nairobi and Mombasa, separated by >400 km, showed greater maternal genetic similarity than expected under isolation-by-distance, a pattern that may reflect gene flow along transportation corridors. Conversely, Ukunda, around 30 km from Mombasa, was comparatively divergent, and populations in Western Kenya were genetically distinct. We found no evidence of non-African ancestry in mtDNA from Rabai or Mombasa despite its previous detection in the nuclear genomes of these populations. Instead, a subset of samples from Marigat and Ukunda showed the closest maternal affinity to West African and non-African lineages. Insecticide assays revealed high susceptibility to bendiocarb, deltamethrin, and fenitrothion across populations, but substantial resistance to permethrin, particularly at coastal sites. Genotyping of the kdr 1534C allele showed the highest resistance allele frequencies in coastal populations, broadly consistent with the phenotypic patterns. This variation in resistance was not associated with mitochondrial ancestry, suggesting that local selection pressures rather than shared maternal ancestry may be shaping resistance. Together, these findings describe the maternal genetic structure of Ae. aegypti in Kenya and show that localised resistance evolution, in the absence of organised Ae. aegypti-targeted control, underscores the need to monitor resistance mechanisms. - Source: PubMed
Publication date: 2026/09/08
Musimbi BrendaHickson SandyMilugo Trizah KRobinson-Rice EleanorOsalla JosephineRotich GilbertJiggins FrankTchouassi David P - Undifferentiated pleomorphic sarcoma (UPS) is the most common pleomorphic sarcoma, and its genomic landscape has been analysed, albeit in small numbers. This study aimed to clarify the relationship between gene variants and the prognosis of patients with advanced UPS. - Source: PubMed
Publication date: 2026/09/07
Kobayashi HiroshiIkegami MasachikaZhang LiuzheOkajima KoichiAndo ToshihikoHirai ToshihideTsuda YusukeTanaka Sakae