Synergistic cooperation of Sall4 and Cyclin D1 in transcriptional repression

被引：24

作者：

Boehm, Johann

Kaiser, Frank J.

Borozdin, Wiktor

Depping, Reinhard

Kohlhase, Juergen ^{[1
]}

机构：

[1] Univ Freiburg, Inst Humangenet & Anthropol, D-7800 Freiburg, Germany

[2] Univ Klinikum Schleswig Holstein, Inst Humangenet, Lubeck, Germany

[3] Univ Lubeck, Inst Physiol, Lubeck, Germany

[4] Praxis Humangenet, D-79100 Freiburg, Germany

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2007年 / 356卷 / 03期

关键词：

SALL4; Okihiro syndrome; zinc finger; nuclear localization; cyclin D1; cell cycle regulation; transcriptional activity;

D O I：

10.1016/j.bbrc.2007.03.050

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Loss of function mutations in SALL4 cause Okihiro syndrome, an autosomal dominant disorder characterised by radial ray malformations associated with Duane anomaly. In zebrafish and mouse Sa114 interacts with TBX5 during limb and heart development and plays a crucial role for embryonic stem (ES) cell pluripotency. Here we report the nuclear interaction of murine Sa114 with Cyclin D1, one of the main regulators of G, to S phase transition in cell cycle, verified by yeast two-hybrid assay, co-immunoprecipitation and intracellular co-localisation. Furthermore, using luciferase reporter gene assays we demonstrate that Sa114 operates as a transcriptional repressor located to heterochromatin and that this activity is modulated by Cyclin D1. (c) 2007 Elsevier Inc. All rights reserved.

引用

收藏

页码：773 / 779

页数：7

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