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。
Phospho-KDR/FLK1(Y996) Antibody
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, IHC-P, E |
|---|---|
| Primary Accession | P35968 |
| Reactivity | Human, Rat, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 151527 Da |
| Gene ID | 3791 |
|---|---|
| Other Names | Vascular endothelial growth factor receptor 2, VEGFR-2, Fetal liver kinase 1, FLK-1, Kinase insert domain receptor, KDR, Protein-tyrosine kinase receptor flk-1, CD309, KDR, FLK1, VEGFR2 |
| Target/Specificity | This KDR/FLK1 Antibody is generated from rabbits immunized with a KLH conjugated synthetic phosphopeptide corresponding to amino acid residues surrounding Y996 of human KDR/FLK1. |
| Dilution | WB~~1:1000 IHC-P~~1:100~500 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Phospho-KDR/FLK1(Y996) Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | KDR (HGNC:6307) |
|---|---|
| Synonyms | FLK1, VEGFR2 |
| 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, such as isoform 2 and isoform 3, may function as decoy receptors for VEGFA, VEGFC and/or VEGFD. Isoform 2 plays an important role as negative regulator of VEGFA- and VEGFC-mediated lymphangiogenesis by limiting the amount of free VEGFA and/or VEGFC and preventing their binding to FLT4. 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. |
| Cellular Location | Cell junction. Endoplasmic reticulum. Cell membrane. Note=Localized with RAP1A at cell-cell junctions (By similarity). Colocalizes with ERN1 and XBP1 in the endoplasmic reticulum in endothelial cells in a vascular endothelial growth factor (VEGF)-dependent manner (PubMed:23529610). {ECO:0000250, ECO:0000269|PubMed:23529610} [Isoform 2]: Secreted. |
| Tissue Location | Detected in cornea (at protein level). Widely expressed. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
KDR (FLK1) is a receptor for VEGF or VEGFC. This protein has a tyrosine-protein kinase activity. The VEGF-kinase ligand/receptor signaling system plays a key role in vascular development and regulation of vascular permeability.
REFERENCES
Le Boeuf, F., et al., J. Biol. Chem. 279(37):39175-39185 (2004).
Lee, Y.K., et al., Blood 104(3):788-794 (2004).
Sulpice, E., et al., Eur. J. Biochem. 271(16):3310-3318 (2004).
Murdaca, J., et al., J. Biol. Chem. 279(25):26754-26761 (2004).
List, A.F., et al., Exp. Hematol. 32(6):526-535 (2004).
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