Relationships of the antiproliferative proteins BTG1 and BTG2 with CAF1, the human homolog of a component of the yeast CCR4 transcriptional complex -: Involvement in estrogen receptor α signaling pathway

Relationships of the antiproliferative proteins BTG1 and BTG2 with CAF1, the human homolog of a component of the yeast CCR4 transcriptional complex -: Involvement in estrogen receptor α signaling pathway
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DOI:
10.1074/jbc.m008201200
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发表时间:
2001-03-30
影响因子:
4.8
通讯作者:
Corbo, L
Corbo, L
中科院分区:
生物学2区
文献类型:
--
作者:
Prévôt, D;Morel, AP;Corbo, L

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我们以前已经报道了B细胞易位基因蛋白(BTG)1和BTG 2与小鼠蛋白质CAF1(CCR 4相关因子1)的物理相互作用,并建议这些蛋白质可能通过与CAF1的结合参与转录调控。在这里,我们描述了在体外和体内的这些蛋白质与hPOP2,人的伴侣hCAF1,BTG蛋白和它们的伴侣hCAF1和hPOP2之间的物理和功能的关系进行了研究,以找出这些相互作用如何影响细胞过程,特别是转录调控。我们定义了它们的相互作用区域,并检测了它们在各种人体组织中的表达。我们还显示了功能数据,表明它们参与雌激素受体α(ER α)介导的转录调控。我们发现,BTG1和BTG2,可能通过它们与CAF1通过CCR4样复合物的相互作用,可以在调节ER α功能中发挥积极或消极的作用。此外,我们的研究结果表明,两个LXXLL基序,称为核受体盒,存在于BTG1和BTG2,参与调节ER α介导的激活。
We have reported previously the physical interaction of B-cell translocation gene proteins (BTG)1 and BTG2 with the mouse protein CAF1 (CCR4-associated factor 1) and suggested that these proteins may participate, through their association with CAF1, in transcription regulation. Here we describe the in vitro and in vivo association of these proteins with hPOP2, the human paralog of hCAF1, The physical and functional relationships between the BTG proteins and their partners hCAF1 and hPOP2 were investigated to find out how these interactions affect cellular processes, and in particular transcription regulation. We defined their interaction regions and examined their expression in various human tissues. We also show functional data indicating their involvement in estrogen receptor a (ER alpha)-mediated transcription regulation. We found that BTG1 and BTG2, probably through their interaction with CAF1 via a CCR4-like complex, can play both positive or negative roles in regulating the ER alpha function. In addition, our results indicate that two LXXLL motifs, referred to as nuclear receptor boxes, present in both BTG1 and BTG2, are involved in the regulation of ER alpha -mediated activation.