• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Molecular and Cellular Biology >Nuclear Receptor Corepressor Recruitment by Unliganded Thyroid Hormone Receptor in Gene Repression during Xenopus laevis Development
【2h】

Nuclear Receptor Corepressor Recruitment by Unliganded Thyroid Hormone Receptor in Gene Repression during Xenopus laevis Development

机译：非洲爪蟾发育过程中未配体甲状腺激素受体在基因抑制中的核受体共募集。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Thyroid hormone receptors (TR) act as activators of transcription in the presence of the thyroid hormone (T3) and as repressors in its absence. While many in vitro approaches have been used to study the molecular mechanisms of TR action, their physiological relevance has not been addressed. Here we investigate how TR regulates gene expression during vertebrate postembryonic development by using T3-dependent amphibian metamorphosis as a model. Earlier studies suggest that TR acts as a repressor during premetamorphosis when T3 is absent. We hypothesize that corepressor complexes containing the nuclear receptor corepressor (N-CoR) are key factors in this TR-dependent gene repression, which is important for premetamorphic tadpole growth. To test this hypothesis, we isolated Xenopus laevis N-CoR (xN-CoR) and showed that it was present in pre- and metamorphic tadpoles. Using a chromatin immunoprecipitation assay, we demonstrated that xN-CoR was recruited to the promoters of T3 response genes during premetamorphosis and released upon T3 treatment, accompanied by a local increase in histone acetylation. Furthermore, overexpression of a dominant-negative N-CoR in tadpole tail muscle led to increased transcription from a T3-dependent promoter. Our data indicate that N-CoR is recruited by unliganded TR to repress target gene expression during premetamorphic animal growth, an important process that prepares the tadpole for metamorphosis.
机译：甲状腺激素受体（TR）在存在甲状腺激素（T3）时起转录激活剂的作用，在没有甲状腺激素（T3）时起阻遏剂的作用。尽管许多体外方法已用于研究TR作用的分子机制，但尚未解决它们的生理相关性。在这里，我们通过使用T3依赖的两栖类变态作为模型，研究TR如何在脊椎动物胚胎后发育过程中调节基因表达。较早的研究表明，当T3缺失时，TR在变态前期可作为阻遏物。我们假设包含核受体corepressor（N-CoR）的corepressor复合物是这种TR依赖的基因阻遏的关键因素，这对变质前growth的生长很重要。为了检验该假设，我们分离了非洲爪蟾N-CoR（xN-CoR），并证明它存在于前t和变态t中。使用染色质免疫沉淀测定法，我们证明xN-CoR在变态前期被募集到T3反应基因的启动子并在T3处理后释放，并伴随着组蛋白乙酰化的局部增加。此外，t尾肌中显性负性N-CoR的过度表达导致依赖T3的启动子转录增加。我们的数据表明，N-CoR由未配体的TR募集以抑制变态前动物生长过程中的靶基因表达，这是为变态准备the的重要过程。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号