Overview |
bs-3347R-PerCP-Cy5.5 |
PRK1 (Thr774)/PRK2 (Thr816) Antibody, PerCP-Cy5.5 Conjugated |
IF(IHC-P), IF(IHC-F), IF(ICC) |
Human, Mouse, Rat, Dog, Cow, Pig, Horse, Rabbit |
Specifications |
PerCP-Cy5.5 |
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 (pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
Store at -20°C. Aliquot into multiple vials to 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 |
IF(IHC-P) |
1:50-200 |
IF(IHC-F) |
1:50-200 |
IF(ICC) |
1:50-200 |