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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Activation of mitogen-activated protein kinases by vascular endothelial growth factor and basic fibroblast growth factor in capillary endothelial cells is inhibited by the antiangiogenic factor 16-kDa N-terminal fragment of prolactin.
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Activation of mitogen-activated protein kinases by vascular endothelial growth factor and basic fibroblast growth factor in capillary endothelial cells is inhibited by the antiangiogenic factor 16-kDa N-terminal fragment of prolactin.

机译:催乳素的抗血管生成因子16-kDa N-末端片段可抑制毛细血管内皮细胞中血管内皮生长因子和碱性成纤维细胞生长因子对促分裂原活化蛋白激酶的激活。

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摘要

A number of factors both stimulating and inhibiting angiogenesis have been described. In the current work, we demonstrate that the angiogenic factor vascular endothelial growth factor (VEGF) activates mitogen-activated protein kinase (MAPK) as has been previously shown for basic fibroblast growth factor. The antiagiogenic factor 16-kDa N-terminal fragment of human prolactin inhibits activation of MAPK distal to autophosphorylation of the putative VEGF receptor, Flk-1, and phospholipase C-gamma. These data show that activation and inhibition of MAPK may play a central role in the control of angiogenesis.
机译:已经描述了许多刺激和抑制血管生成的因素。在当前的工作中,我们证明了血管生成因子血管内皮生长因子(VEGF)激活有丝分裂原激活的蛋白激酶(MAPK),正如先前对碱性成纤维细胞生长因子所显示的那样。人催乳素的抗血管生成因子16-kDa N端片段可抑制假定的VEGF受体,Flk-1和磷脂酶C-γ自身磷酸化远端的MAPK活化。这些数据表明,MAPK的激活和抑制可能在血管生成的控制中起着核心作用。

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