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Roles of old players in the suppression of a new player: networks for the transcriptional control of angiogenesis.

机译:老玩家在抑制新玩家中的作用:用于血管生成转录控制的网络。

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摘要

During the formation of blood vessels, Id1, a member of the helix-loop-helix (HLH) family, and TAL1/SCL, a basic HLH (bHLH) transcription factor, play important roles in the activation of endothelial cells. Recent reports revealed that E2-2, another bHLH transcription factor, inhibits angiogenesis in vitro and in vivo by suppressing the expression of vascular endothelial growth factor receptor 2 (VEGFR2). Id1 and TAL1/SCL dimerize with E2-2 and relieve the E2-2-mediated down-regulation of VEGFR2 expression, leading to the activation of endothelial cells. These findings reveal a novel interplay between HLH transcription factors that regulate angiogenesis.
机译:在血管形成过程中,螺旋环-螺旋(HLH)家族成员Id1和碱性HLH(bHLH)转录因子TAL1 / SCL在内皮细胞激活中起重要作用。最近的报道显示,另一种bHLH转录因子E2-2通过抑制血管内皮生长因子受体2(VEGFR2)的表达在体外和体内抑制血管生成。 Id1和TAL1 / SCL与E2-2二聚,并缓解E2-2介导的VEGFR2表达下调,从而激活内皮细胞。这些发现揭示了调节血管生成的HLH转录因子之间的新型相互作用。

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