Regulation of the helix-loop-helix proteins, E2A and Id3, by the Ras-ERK MAPK cascade
Regulation of the helix-loop-helix proteins, E2A and Id3, by the Ras-ERK MAPK cascade
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DOI：
10.1038/84273
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发表时间：
2001-02-01
影响因子：
30.5
通讯作者：
Murre, C
中科院分区：
文献类型：
--
作者：
Bain, G;Cravatt, CB;Murre, C
丝裂原活化蛋白激酶（MAPK）途径的活化导致多种细胞类型（包括发育中的胸腺细胞）中的细胞分化和/或增殖。碱性螺旋-环-螺旋（bHLH）蛋白E12和E47以及抑制剂HLH蛋白Id 3在胸腺细胞分化中起关键作用。我们在这里表明，E2 A DNA结合降低初级未成熟胸腺细胞继T细胞受体（TCR）介导的连接。尽管E2 A mRNA和蛋白质的表达未改变，但Id 3转录物在来自TCR的信号传导后被快速诱导。Id 3转录的激活受细胞外信号调节激酶（ERK）MAPK模块以剂量依赖性方式调节。这些观察结果直接将ERK MAPK级联和HLH蛋白以线性途径连接。
Activation of mitogen-activated protein kinase (MAPK) pathways leads to cellular differentiation and/or proliferation in a wide variety of cell types, including developing thymocytes. The basic helix-loop-helix (bHLH) proteins E12 and E47 and an inhibitor HLH protein, Id3, play key roles in thymocyte differentiation. We show here that E2A DNA binding is lowered in primary immature thymocytes consequent to T cell receptor (TCR)-mediated ligation. Whereas expression of E2A mRNA and protein are unaltered, Id3 transcripts are rapidly induced upon signaling from the TCR. Activation of Id3 transcription is regulated in a dose-dependent manner by the extracellular signal-regulated kinase (ERK) MAPK module. These observations directly connect the ERK MAPK cascade and HLH proteins in a linear pathway.