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体内核小体介导的转录因子 - 染色质起始复合物在小鼠乳腺肿瘤病毒长末端重复序列处的破坏

Nucleosome-mediated disruption of transcription factor-chromatin initiation complexes at the mouse mammary tumor virus long terminal repeat in vivo.

作者信息

Lee H L, Archer T K

机构信息

Department of Obstetrics & Gynecology, University of Western Ontario, London, Canada.

出版信息

Mol Cell Biol. 1994 Jan;14(1):32-41. doi: 10.1128/mcb.14.1.32-41.1994.

Abstract

Glucocorticoid induction of mouse mammary tumor virus (MMTV) is short lived, returning to base levels within 24 h despite the continued presence of hormone. MMTV DNA sequences assembled as chromatin require hormone for binding by nuclear factor 1 (NF1) and octamer proteins (OCT). However, in the same cells, NF1 and OCT factors are bound to transiently introduced DNA in the absence of hormone. In contrast, recruitment of the TATA-binding protein and a novel DNA-binding protein, which we have designated FDT, for factor downstream of the TATA-binding protein, is hormone dependent for both stable and transient templates. Furthermore, transient DNA templates, but not nucleosomal templates, retain these transcription factors over the course of 24 h. This finding suggests that MMTV chromatin structure contributes to activation and cessation of transcription in vivo.

摘要

糖皮质激素对小鼠乳腺肿瘤病毒(MMTV)的诱导作用持续时间较短,尽管激素持续存在,但在24小时内会恢复到基础水平。组装成染色质的MMTV DNA序列需要激素才能被核因子1(NF1)和八聚体蛋白(OCT)结合。然而,在相同的细胞中,在没有激素的情况下,NF1和OCT因子会与瞬时导入的DNA结合。相比之下,TATA结合蛋白和一种新的DNA结合蛋白(我们将其命名为FDT,即TATA结合蛋白下游的因子)的募集,对于稳定和瞬时模板而言都依赖于激素。此外,瞬时DNA模板而非核小体模板在24小时内会保留这些转录因子。这一发现表明,MMTV染色质结构有助于体内转录的激活和终止。

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