| Overview |
| bs-3347R-Biotin |
| PRK1 (Thr774)/PRK2 (Thr816) Antibody, Biotin Conjugated |
| ELISA, IHC-P, IHC-F |
| Human, Mouse, Rat, Dog, Cow, Pig, Horse, Rabbit |
| Specifications |
| Biotin |
| Rabbit |
| KLH conjugated synthetic phosphopeptide derived from human PRK1 around the phosphorylation site of Thr774 |
| Thr816 |
| Polyclonal |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| Store at -20°C for 12 months. |
| Target |
| 5585 |
| Cytoplasm, Nucleus, Cell membrane |
| Prokineticin-1/Endocrine-gland-derived vascular endothelial growth factor; PROK1; EGVEGF; PK1; EG-VEGF; PRK1. |
| Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) induces proliferation, migration, and fenestration in capillary endothelial cells derived from endocrine glands. EG-VEGF possesses an HIF-1 binding site; its expression is induced by hypoxia and restricted to the steroidogenic glands (ovary, testis, adrenal and placenta). Expression of EG-VEGF is often complementary to the expression of VEGF, suggesting that these molecules function in a coordinated manner. EG-VEGF is an example of a class of highly specific mitogens that act to regulate proliferation and differentiation of the vascular endothelium in a tissue-specific manner. It is expressed primarily in one type of tissue and acts selectively on one type of endothelium. EG-VEGF, possibly through binding to a G protein-coupled receptor, results in the activation of MAPK p44/42 and phosphatidylinositol 3-kinase signaling pathways, leading to proliferation, migration and survival of responsive endothelial cells . |
| Application Dilution |
| ELISA |
1:500-1000 |
| IHC-P |
1:200-400 |
| IHC-F |
1:100-500 |
Powered by Bioz