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Angiogenesis inhibitor. Additionally we are shipping Vasohibin 1 Antibodies (67) and Vasohibin 1 Proteins (5) and many more products for this protein.
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VASH1 expression inhibited tumor vascularization and growth, not only in high VEGF (show VEGFA ELISA Kits)-producing cells, but also in high PDGF (show PDGFA ELISA Kits)-producing cells, reduced their peritoneal dissemination and ascites, and prolonged the survival time of the host
in this study, the length of tube forming structures of endothelial cells in vitro showed that Vasohibin-1 expression in gastric cancer cells significantly decreased the ability of vessel formation of endothelium cells.
These results indicate that cancer cells proteolytically inactivate VASH1 protein secreted by ECs in the tumour microenvironment
VASH1 exerts an antitumor effect on ovarian cancer by inhibiting angiogenesis in the tumor environment
VASH1 expression levels in atheroma reflects both enhanced neovascularization and the inflammatory burden
Knockdown of VASH1 in cancer cells promoted cell growth, adhesion and migration in vitro, and enhanced tumorigenesis and metastasis in vivo.
VASH1 and VASH2 showed distinctive localization and opposing function on the fetoplacental vascularization.
These results suggest that the renal levels of VASH-1 may be affected by local inflammation, crescentic lesions and VEGFR-2 (show KDR ELISA Kits).
High VASH1 expression is associated with non-small cell lung cancer.
Overexpression of VASH1 in CRC (show CALR ELISA Kits) cells increased malignant potential and promoted metastasis.
Unaffected fibrosis and angiogenesis seen by knocking out endogenous vasohibin-1.
endogenous VASH1 may regulate the development of diabetic renal alterations
PKCdelta (show PKCd ELISA Kits) deficiency enhances neointimal formation, which is associated with delayed reendothelialization and involves increased cellular vasohibin-1 accumulation.
vasohibin1 is the first known intrinsic factor (show GIF ELISA Kits) having broad-spectrum antilymphangiogenic activity
These results suggest a role for VASH1 in negative feedback regulation of haematopoietic progenitors proliferation during recovery following bone marrow ablation.
Loss of vasohibin-1 is associated with persistent angiogenesis in the termination zone of endothelial cells.
These results suggest that endogenous vasohibin-1 is involved in tumor angiogenesis and exogenous vasohibin-1 blocks sprouting angiogenesis by tumors, matures the remaining vessels, and enhances the antitumor effect of conventional chemotherapy
Overexpression of murine VASH1 inhibited angiogenic sprouting and supports vascular maturation processes in vivo.
results demonstrate expression of VASH1, especially in blood vascular endothelial cells in the corpus luteum (CL) and show VASH1 inhibits VEGFA (show VEGFA ELISA Kits)-stimulated capillary like-tube formation by luteal endothelial cells and lymphatic endothelial cells vitro; results indicate VASH1 may act as a negative feedback regulator of angiogenesis and lymphangiogenesis in the CL
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.