VEGFR2 Antibody (Ab_1214), pAb, Rabbit
- Known as:
- VEGFR2 Antibody (Ab_1214), pAb, Rabbit
- Catalog number:
- A00355
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- VEGFR2 Antibody (Ab_1214) pAb Rabbit
Ask about this productRelated genes to: VEGFR2 Antibody (Ab_1214), pAb, Rabbit
- 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 Antibody (Ab_1214), pAb, Rabbit
Related articles to: VEGFR2 Antibody (Ab_1214), pAb, Rabbit
- Angiosarcoma is a poorly understood sarcoma due to its high heterogeneity and rarity. Here we show a comprehensive clinical and molecular analysis of a large cohort of 254 angiosarcoma patients through the patient-partnered Angiosarcoma Project. By integrating transcriptomic, somatic, and germline variant data, we find that subcutaneous angiosarcomas frequently exhibit TGF-β and receptor tyrosine kinase signaling upregulation, with driver mutations in KDR, PLCG1, and POT1. Meanwhile, cutaneous angiosarcomas are enriched for MYC-driven programs, UV mutational signatures, immune checkpoint gene expression, and TP53, FLT4, and BRAF mutations. Germline POT1 pathogenic variant carriers have a 92.7-fold higher risk of developing angiosarcoma, with 'double-hit' germline and somatic variant carriers developing disease decades earlier. Additionally, POT1-mutated tumors underexpress TERT and overexpress CHAMP1. Altogether, these findings elucidate the molecular framework of angiosarcoma, nominate therapeutic targets, and highlight the power of direct patient engagement in rare cancers. - Source: PubMed
Publication date: 2026/07/24
Chu HoyinHollyer MarissaBorden Brittany AReilly Christopher RGómez Tejeda Zañudo JorgeThomas Beena SPhelps KolbePimenta Erica MariaHan SeunghunCamp Sabrina YGillani RiazGutierrez JacobLareau Caleb ANagy MatthewJohnson JeremyAlao OyinGrundman HadleySterlin LaurenTerzi WillSosa DeliaSmall Ilan KMcGillicuddy MaryAlharbi NoufAnastasio ElanaChastain ParkerBhakhri PriyankaHornick Jason LChoudhry HaniDiehl Diane MVan Allen Eliezer MWagle NikhilPainter Corrie AAlDubayan Saud - Cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) is a common female malignancy. Gut microbiota and metabolites are critical regulators of tumor immunity and therapy, but their roles in CESC remain unclear. This study integrated TCGA and GEO datasets with gut microbiota information to construct a protein-protein interaction network. These targets were prioritized using machine learning, SHAP interpretation, and Mendelian randomization analysis. Immune-related pathways were explored using single-cell and spatial transcriptomic analyses. Molecular docking and molecular dynamics simulations were performed to evaluate potential interactions between key metabolites and their targets. A total of 136 gut microbiota-related DEGs were identified, which may be associated with intercellular immune interactions. KDR was selected as a core target and may exert protective effects. Single-cell and spatial transcriptomic analyses suggested that specific metabolites may be associated with changes in the tumor microenvironment potentially involving the MIF signaling pathway. Network analysis of microbes, metabolites, and targets suggested that metabolites such as 5-(3,4-dihydroxyphenyl) pentanoic acid may serve as key mediators linking gut microbiota and KDR signaling. Additionally, eight non-toxic metabolites with favorable drug-likeness were identified, molecular docking and molecular dynamics simulation demonstrated stable binding to KDR with potential bioactivity, providing a theoretical basis for developing microbiota-related therapeutic strategies. The gut microbiota and its metabolites may be associated with the immune microenvironment and tumor progression in CESC, potentially involving the MIF signaling axis. This study provides a computational framework and preliminary evidence supporting microbiota-related hypotheses, and may inform future experimental investigations and therapeutic strategy development. - Source: PubMed
Publication date: 2026/08/25
Chen BinXu Changchang - Glioblastoma isocitrate dehydrogenase (IDH)-wildtype (GBM) has been reclassified based on molecular and phenotypic features. Intratumoral hemorrhage is a phenotypic subtype with poorly understood molecular and clinical characteristics. We aimed to characterize the molecular profile and outcomes of hemorrhagic glioblastoma (hGBM) compared with non-hGBM. - Source: PubMed
Publication date: 2026/08/24
Bueno AngelDono AntonioAlcantar OscarAmezquita-Contreras ChristianOcasio LauraHsu SigmundAmsbaugh MarkZhu Jay-JiguangBlanco Angel IRiascos Roy FBallester Leomar YTandon NitinEsquenazi Yoshua - 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
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