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Merck
CN

676474

Sigma-Aldrich

VEGF₁₆₄, Mouse, Recombinant, S. frugiperda

别名:

Vascular Endothelial Growth Factor₁₆₄

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UNSPSC代码:
12352202
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方案

≥95% (SDS-PAGE)

质量水平

表单

lyophilized solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze

运输

wet ice

储存温度

−70°C

一般描述

Recombinant, mouse VEGF164 (164-amino acid splice variant of VEGF) expressed in S. frugiperda insect cells. It is the most abundant form of VEGF found in mice. VEGF164 is a potent angiogenic factor and vascular permeability factor in vivo, as well as a chemoattractant for monocytes and endothelial cells. Forms a biological active homodimer. Evidence also suggests that it is biologically active as a heterodimer with other VEGF splice variants.
Recombinant, mouse VEGF164 (164-amino acid splice variant of VEGF) expressed in S. frugiperda insect cells. The most abundant form in mice, VEGF164 is a potent angiogenic factor and vascular permeability factor in vivo, as well as a chemoattractant for monocytes and endothelial cells. Forms a biologically active homodimer and evidence suggests that it is also biologically active as a heterodimer with other VEGF splice variants. Expression of VEGF164 appears to be essential for normal bone development and vascularization.

生化/生理作用

ED₅₀ ≥1 ng/ml as measured by the stimulation of ³H-thymidine incorporation by human umbilical vein endothelial cells and bovine aortic endothelial cells. In vivo effects using the 13-day-old chick chorioallantoic membrane (CAM) assay can be seen between 0.5-4 µg

制备说明

Following reconstitution, aliquot and freeze (-70°C). Stock solutions are stable for up to 3 months at -70°C.
Reconstitute in PBS or 50 mM acetic acid to a concentration ≥ 100 ng/µl.

其他说明

Maes, C., et al. 2002. Mech. Dev.111, 61.
Grunstein, J., et al. 2000. Mol. Cell Biol.20, 7282.
Springer, M.L., et al. 2000. J. Gene Med.2, 279.

法律信息

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

免责声明

Toxicity: Standard Handling (A)

储存分类代码

10-13 - German Storage Class 10 to 13

法规信息

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Kai Fang et al.
International journal of inflammation, 2020, 6150942-6150942 (2020-03-06)
It has been reported that pathological angiogenesis contributes to both experimental colitis and inflammatory bowel disease. Recently, we demonstrated that endothelial caveolin-1 plays a key role in the pathological angiogenesis of dextran sodium sulfate (DSS) colitis. However, the molecular mechanism

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