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由甲状腺激素反应元件144介导的负转录调控需要多价因子CTCF与一个新的靶DNA序列结合。

Negative transcriptional regulation mediated by thyroid hormone response element 144 requires binding of the multivalent factor CTCF to a novel target DNA sequence.

作者信息

Awad T A, Bigler J, Ulmer J E, Hu Y J, Moore J M, Lutz M, Neiman P E, Collins S J, Renkawitz R, Lobanenkov V V, Filippova G N

机构信息

Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA.

出版信息

J Biol Chem. 1999 Sep 17;274(38):27092-8. doi: 10.1074/jbc.274.38.27092.

Abstract

DNA target sites for a "multivalent" 11-zinc-finger CCTC-binding factor (CTCF) are unusually long ( approximately 50 base pairs) and remarkably different. In conjunction with the thyroid receptor (TR), CTCF binding to the lysozyme gene transcriptional silencer mediates the thyroid hormone response element (TRE)-dependent transcriptional repression. We tested whether other TREs, which in addition to the presence of a TR binding site require neighboring sequences for transcriptional function, might also contain a previously unrecognized binding site(s) for CTCF. One such candidate DNA region, previously isolated by Bigler and Eisenman (Bigler, J., and Eisenman, R. N. (1995) EMBO J. 14, 5710-5723), is the TRE-containing genomic element 144. We have identified a new CTCF target sequence that is adjacent to the TR binding site within the 144 fragment. Comparison of CTCF recognition nucleotides in the lysozyme silencer and in the 144 sequences revealed both similarities and differences. Several C-terminal CTCF zinc fingers contribute differently to binding each of these sequences. Mutations that eliminate CTCF binding impair 144-mediated negative transcriptional regulation. Thus, the 144 element provides an additional example of a functionally significant composite "TRE plus CTCF binding site" regulatory element suggesting an important role for CTCF in cooperation with the steroid/thyroid superfamily of nuclear receptors to mediate TRE-dependent transcriptional repression.

摘要

一种“多价”的11锌指CCTC结合因子(CTCF)的DNA靶位点异常长(约50个碱基对)且差异显著。与甲状腺受体(TR)结合后,CTCF与溶菌酶基因转录沉默子的结合介导了甲状腺激素反应元件(TRE)依赖性的转录抑制。我们测试了其他TREs,除了存在TR结合位点外,其转录功能还需要相邻序列,是否也可能包含一个以前未被识别的CTCF结合位点。一个这样的候选DNA区域,先前由Bigler和Eisenman分离得到(Bigler, J., and Eisenman, R. N. (1995) EMBO J. 14, 5710 - 5723),是含有TRE的基因组元件144。我们在144片段中鉴定出一个与TR结合位点相邻的新的CTCF靶序列。比较溶菌酶沉默子和144序列中的CTCF识别核苷酸,发现了异同之处。几个CTCF C末端锌指对这些序列各自结合的贡献不同。消除CTCF结合的突变会损害144介导的负转录调控。因此,144元件提供了一个功能上重要的复合“TRE加CTCF结合位点”调控元件的额外例子,表明CTCF在与核受体的类固醇/甲状腺超家族合作介导TRE依赖性转录抑制中发挥重要作用。

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