| Overview |
| bs-3347R |
| Phospho-PRK1 (Thr774) + PRK2 (Thr816) + PRK3 (Thr718) Polyclonal Antibody |
| ELISA, IHC-P, IHC-F, IF(IHC-P), IF(IHC-F), IF(ICC) |
| Human, Mouse, Rat, Dog, Cow, Pig, Horse, Rabbit |
| Specifications |
| Unconjugated |
| Rabbit |
| KLH conjugated synthetic phosphopeptide derived from human PRK1 around the phosphorylation site of Thr774 |
| Thr816 |
| Polyclonal |
| #REF! |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| 0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| Shipped at 4_. Store at -20_ for one year. Avoid repeated freeze/thaw cycles. |
| 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 |
| IF(IHC-P) |
1:50-200 |
| IF(IHC-F) |
1:50-200 |
| IF(ICC) |
1:50-200 |
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