癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
Anti-VEGFR2/KDR Antibody
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Application 
| IHC-F |
|---|---|
| Primary Accession | O08775 |
| Host | Mouse |
| Isotype | Mouse IgG1 |
| Reactivity | Human |
| Clonality | Monoclonal |
| Format | Lyophilized |
| Description | Mouse IgG monoclonal antibody for VEGFR2, kinase insert domain receptor (a type III receptor tyrosine kinase) (KDR) detection. Tested with IHC-F in Human. No cross reactivity with other proteins. |
| Reconstitution | Add 1ml of PBS buffer will yield a concentration of 100ug/ml. |
| Gene ID | 25589 |
|---|---|
| Other Names | Vascular endothelial growth factor receptor 2, VEGFR-2, 2.7.10.1, Fetal liver kinase 1, FLK-1, Protein-tyrosine kinase receptor flk-1, CD309, Kdr, Flk1 |
| Calculated MW | 150394 Da |
| Application Details | Immunohistochemistry(Frozen Section), 1-2 µg/ml, Human |
| Subcellular Localization | Cell membrane ; Single-pass type I membrane protein . Cytoplasm . Nucleus . Cytoplasmic vesicle . Early endosome . Cell junction . Endoplasmic reticulum . Detected on caveolae-enriched lipid rafts at the cell surface. Is recycled from the plasma membrane to endosomes and back again. Phosphorylation triggered by VEGFA binding promotes internalization and subsequent degradation. VEGFA binding triggers internalization and translocation to the nucleus. Localized with RAP1A at cell-cell junctions. Colocalizes with ERN1 and XBP1 in the endoplasmic reticulum in endothelial cells in a vascular endothelial growth factor (VEGF)-dependent manner (By similarity). . |
| Tissue Specificity | Expressed in the post-pubertal mammary glands. . |
| Source | Eukaryota |
| Protein Name | Vascular endothelial growth factor receptor 2 |
| Contents | Mouse ascites fluid, 1.2% sodium acetate, 2mg BSA, with 0.01mg NaN3 as preservative. |
| Clone Names | KDR-1 |
| Immunogen | Recombinant human extracellular domain of VEGFR-2(KDR). |
| Purification | Ascites |
| Cross Reactivity | No cross reactivity with other proteins |
| Storage | At -20˚C for one year. After r˚Constitution, at 4˚C for one month. It˚Can also be aliquotted and stored frozen at -20˚C for a longer time.Avoid repeated freezing and thawing. |
| Sequence Similarities | Belongs to the protein kinase superfamily. Tyr protein kinase family. CSF-1/PDGF receptor subfamily. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | Kdr {ECO:0000312|RGD:2965} |
|---|---|
| Synonyms | Flk1 |
| Function | Tyrosine-protein kinase that acts as a cell-surface receptor for VEGFA, VEGFC and VEGFD. Plays an essential role in the regulation of angiogenesis, vascular development, vascular permeability, and embryonic hematopoiesis. Promotes proliferation, survival, migration and differentiation of endothelial cells. Promotes reorganization of the actin cytoskeleton. Isoforms lacking a transmembrane domain may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Modulates FLT1 and FLT4 signaling by forming heterodimers. Binding of vascular growth factors to isoform 1 leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol-1,4,5- trisphosphate and the activation of protein kinase C. Mediates activation of MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Mediates phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, reorganization of the actin cytoskeleton and activation of PTK2/FAK1. Required for VEGFA-mediated induction of NOS2 and NOS3, leading to the production of the signaling molecule nitric oxide (NO) by endothelial cells. Phosphorylates PLCG1. Promotes phosphorylation of FYN, NCK1, NOS3, PIK3R1, PTK2/FAK1 and SRC (By similarity). |
| Cellular Location | Cell membrane {ECO:0000250|UniProtKB:P35968}; Single-pass type I membrane protein. Cytoplasm. Nucleus. Cytoplasmic vesicle. Early endosome. Cell junction. Endoplasmic reticulum {ECO:0000250|UniProtKB:P35968} Note=Detected on caveolae-enriched lipid rafts at the cell surface. Is recycled from the plasma membrane to endosomes and back again Phosphorylation triggered by VEGFA binding promotes internalization and subsequent degradation. VEGFA binding triggers internalization and translocation to the nucleus. Localized with RAP1A at cell-cell junctions. Colocalizes with ERN1 and XBP1 in the endoplasmic reticulum in endothelial cells in a vascular endothelial growth factor (VEGF)- dependent manner (By similarity). {ECO:0000250|UniProtKB:P35968} |
| Tissue Location | Expressed in the post-pubertal mammary glands. |
Research Areas
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
VEGF, a homodimeric glycoprotein of relative molecular mass 45,000, is the only mitogen that specifically acts on endothelial cells. The importance of VEGF and its receptor system in tumor growth and intervention in this system may provide promising approaches to cancer therapy. VEGF receptor 2 is a member of a receptor tyrosine kinase family. Like other growth factor receptors, upon ligand binding VEGF receptor 2 dimerises and is autophosphorylated on multiple tyrosine residues.
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