|Application ||WB, IHC-P, IF, E|
|Other Accession||NP_055724, 7662454|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||40957 Da|
|Application Notes||VASH1 antibody can be used for detection of VASH1 by Western blot at 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Target/Specificity||VASH1; VASH1 antibody is predicted to not cross-react with other vasohibin protein family members. At least two isoforms are known to exist; this antibody will recognize only the long isoform.|
|Reconstitution & Storage||VASH1 antibody can be stored at 4 ℃, stable for one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||VASH1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Angiogenesis inhibitor. Inhibits migration, proliferation and network formation by endothelial cells as well as angiogenesis. This inhibitory effect is selective to endothelial cells as it does not affect the migration of smooth muscle cells or fibroblasts. Does not affect the proliferation of cancer cells in vitro, but inhibits tumor growth and tumor angiogenesis. Acts in an autocrine manner. Inhibits artery neointimal formation and macrophage infiltration. Exhibits heparin-binding activity.|
|Tissue Location||Preferentially expressed in endothelial cells. Highly expressed in fetal organs. Expressed in brain and placenta, and at lower level in heart and kidney. Highly detected in microvessels endothelial cells of atherosclerotic lesions|
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Provided below are standard protocols that you may find useful for product applications.
VASH1 Antibody: VASH1 was originally identified as an endothelium-derived vascular endothelial growth factor (VEGF)-inducible angiogenesis inhibitor that acts in a negative feedback manner. VASH1 mRNA is expressed brain, heart, kidney and placenta in the adult, with robust expression in various organs during embryonic development. VASH1 expression in tumor cells and tumor vasculature is silenced by methylation by increased expression of Zeste homolog 2 (EZH2). The increase of EZH2 expression is induced by VEGF stimulation, leading to poor clinical prognosis. Recombinant adenovirus expressing VASH prevented tumor angiogenesis and inhibited tumor growth, suggesting that it may be a potentially valuable antitumor therapy in the clinic.
Watanabe K, Hasegawa Y, Yamashita H, et al. Vasohibin as an endothelium-derived negative feedback regulator of angiogenesis. J. Clin. Invest. 2004; 114:989-907
Lu C, Han HD, Mangala LS, et al. Regulation of tumor angiogenesis by EZH2. Cancer Cell 2010; 18:185-97.
Li D, Zhou K, Wang S, et al. Recombinant adenovirus encoding vasohibin prevents tumor angiogenesis and inhibits tumor growth. Cancer Sci. 2010; 101:448-52.
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