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Endostatin is able to avoke non-uniform response for proliferation, cell mount and migration of entothelial cells, which different endostatin binding characteristic, leads to the assumption that endostatin effect is strongly dependent from endothelial cell type. Furthermore endostatin inhibits angiogenesis and tumor growth in vivo by inducing apoptosis in endothelial cells. The local delivery of endostatin seems to specifically affect tumor-associated microvessels by reduction of the vessel density, diameter and functionality. Tumor cell migration and invasion was greatly reduced in the endostatin treated animals. Endostatin is non-toxic and does not induce aquired drug resistance and has therefor become a potent new therapy strategy in solid neoplasias. This therapy appears to have a high potential not only for the treatment of gliomas, the most common brain tumors, but also in other tumors. The ability of endostatin to inhibit neoangiogenesis is mediated, at least in part, by Zn^+2 binding and elastase processing. Widespread endostatin expression was found in elactic fibers in vessel walls and in some other basement membrane zones. Endostatin is released by neurons to accumulate in amyloid plaques in Alzheimer's disease.
antiangiogenic agent; Col18a1; Collagen alpha-1(XVIII) chain; collagen type XVIII alpha 1 chain; collagen, type XVIII, alpha 1; endostatin; FLJ27325; FLJ34914; KNO; KNO1; KS; MGC74745; multi-functional protein MFP; NC1; Non-collagenous domain 1; procollagen, type XVIII, alpha 1
100 µg
100 µg
150 µL
100 µg
100 µg
100 µL
100 µL
100 µL
100 µg
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