Datta P K, Raychaudhuri P, Bagchi S
Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago 60612, USA.
Mol Cell Biol. 1995 Oct;15(10):5444-52. doi: 10.1128/MCB.15.10.5444.
The retinoblastoma-related protein p107 has been shown to be a regulator of the transcription factor E2F. p107 associates with E2F via its pocket region and represses E2F-dependent transcription. In this study, we provide evidence for a novel interaction between p107 and the transcription factor Sp1. We show that p107 can be found endogenously associated with Sp1 in the extracts of several different cell lines. Moreover, in transient transfection assays, expression of p107 represses Sp1-dependent transcription. This repression of Sp1-dependent transcription does not require the DNA-binding domain of Sp1. Transcription driven by a chimeric protein containing the Ga14 DNA-binding domain and the Sp1 activation domains is inhibited by p107. Interestingly, unlike the repression of E2F-dependent transcription, the repression of Sp1-dependent transcription does not depend on an intact pocket region. We show that distinct regions of p107 are involved in the control of Sp1 and E2F.
视网膜母细胞瘤相关蛋白p107已被证明是转录因子E2F的一种调节因子。p107通过其口袋区域与E2F结合,并抑制E2F依赖的转录。在本研究中,我们提供了p107与转录因子Sp1之间存在新型相互作用的证据。我们发现,在几种不同细胞系的提取物中,p107可内源性地与Sp1结合。此外,在瞬时转染实验中,p107的表达可抑制Sp1依赖的转录。这种对Sp1依赖转录的抑制并不需要Sp1的DNA结合结构域。由包含Gal4 DNA结合结构域和Sp1激活结构域的嵌合蛋白驱动的转录受到p107的抑制。有趣的是,与对E2F依赖转录的抑制不同,对Sp1依赖转录的抑制并不依赖于完整的口袋区域。我们表明,p107的不同区域参与对Sp1和E2F的调控。