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E2F1与E2F4之间DNA结合特性的差异决定了Mcl-1启动子的抑制作用。

Differences in DNA binding properties between E2F1 and E2F4 specify repression of the Mcl-1 promoter.

作者信息

Croxton Rhonda, Ma Yihong, Cress W Douglas

机构信息

Program in Molecular Oncology, H Lee Moffitt Comprehensive Cancer Center and Research Institute, Tampa, Florida, FL 33612, USA.

出版信息

Oncogene. 2002 Feb 28;21(10):1563-70. doi: 10.1038/sj.onc.1205232.

Abstract

E2F1 is a potent inducer of apoptosis whereas its relative, E2F4, generally does not promote cell death. Other work from our laboratory has demonstrated that E2F1 can directly bind and represss the Mcl-1 promoter - contributing to E2F1-mediated apoptosis. Here we show that while E2F1 can repress the Mcl-1 promoter, other members of the E2F family (such as E2F4) cannot. Characterization of the Mcl-1 promoter demonstrates that the -143/+10 region is critical for E2F1-mediated downregulation. We demonstrate that the ability of E2F1 to repress the Mcl-1 promoter correlates with its ability to bind within the required -143/+10 region of this promoter. In contrast, E2F4 is unable to bind to the -143/+10 region of the Mcl-1 promoter. We propose that E2F4 is unable to repress the Mcl-1 promoter primarily as a result of insufficient binding to the essential regulatory region. This is the first evidence of DNA binding specificity among E2F family members that results in differential regulation of a naturally occurring promoter.

摘要

E2F1是一种强大的凋亡诱导因子,而其相关蛋白E2F4通常不会促进细胞死亡。我们实验室的其他研究表明,E2F1可以直接结合并抑制Mcl-1启动子,这有助于E2F1介导的细胞凋亡。在此我们表明,虽然E2F1可以抑制Mcl-1启动子,但E2F家族的其他成员(如E2F4)则不能。对Mcl-1启动子的特征分析表明,-143/+10区域对于E2F1介导的下调至关重要。我们证明,E2F1抑制Mcl-1启动子的能力与其在该启动子所需的-143/+10区域内结合的能力相关。相比之下,E2F4无法结合到Mcl-1启动子的-143/+10区域。我们提出,E2F4无法抑制Mcl-1启动子主要是由于其与关键调控区域的结合不足。这是E2F家族成员之间DNA结合特异性导致对天然存在的启动子进行差异调控的首个证据。

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