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HLH GENE FUNCTION IN NEURONAL CELL DETERMINATION

HLH GENE FUNCTION IN NEURONAL CELL DETERMINATION
HLH 基因在神经细胞测定中的功能
批准号:
7273133
负责人:
Michael A. Caudy
金额:
$2.5万
依托单位国家:
美国
项目类别:
财政年份:
1991
资助国家:
美国
项目状态:
已结题
起止时间:
1991-03-08 至 2007-07-31

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中文摘要
翻译
描述(摘自申请者摘要):在果蝇体内,神经元前体细胞 测定受碱性螺旋-环-螺旋(BHLH)转录调控 各种因素。这些包括神经bHLH激活剂蛋白,如Achaete、Scute 和致命的Scute。缺口介导的侧向抑制过程 信号通路抑制原神经基因的表达。凹槽信令是已知的 导致原神经基因的转录抑制。 这个项目的目标是研究转录后调控。 果蝇的神经基因Achaete、scute和致死的scute。这个 研究人员提供的证据表明,Notch通路的激活也 Achaete原神经蛋白翻译后抑制的结果 通过其C末端转录激活(TA)结构域。一个N端 结构域也强烈地抑制Achaete TA的活性。同源C-端和N-端 结构域在Scute(L的c)蛋白的剑突和致死蛋白中高度保守, 它可能受相同途径的转录后调控。
英文摘要
DESCRIPTION (from applicant's abstract): In Drosophila, neuronal precursor cell determination is regulated by basic Helix-Loop-Helix (bHLH) transcription factors. These include proneural bHLH activator proteins such as Achaete, Scute and Lethal of Scute. A lateral inhibition process mediated by the Notch signaling pathway inhibits proneural gene expression. Notch signaling is known to result in transcriptional repression of proneural genes. The goals of this project are to study the post-transcriptional regulation of the Drosophila proneural genes Achaete, Scute, and Lethal of Scute. The investigator provides evidence that activation of the Notch pathway also results in post-translational inhibition of the Achaete proneural protein through its C-terminal transcriptional activation (TA) domain. An N terminal domain also strongly inhibits Achaete TA activity. Homologous C- and N-terminal domains are highly conserved in the Scute and Lethal of Scute (L'Sc) proteins, which may be post-transcriptionally regulated by the same pathways.
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DOI: 10.1002/(sici)1521-1878(199804)20:4
发表时间: 1998-04
期刊: BioEssays : news and reviews in molecular, cellular and developmental biology
影响因子: --
作者: [L. Johnston]
通讯作者: L. Johnston
GROWTH FACTOR SIGNALS THROUGH BHLH TRANSCRIPTION FACTORS
GROWTH FACTOR SIGNALS THROUGH BHLH TRANSCRIPTION FACTORS
GROWTH FACTOR SIGNALS THROUGH BHLH TRANSCRIPTION FACTORS
GROWTH FACTOR SIGNALS THROUGH BHLH TRANSCRIPTION FACTORS
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