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首页> 外文期刊>Journal of Cellular Physiology >Pin1-mediated Runx2 modification is critical for skeletal development
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Pin1-mediated Runx2 modification is critical for skeletal development

机译：Pin1-mediated Runx2修改是至关重要的骨骼发育

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摘要

Runx2 is the master transcription factor for bone formation. Haploinsufficiency of RUNX2 is the genetic cause of cleidocranial dysplasia (CCD) that is characterized by hypoplastic clavicles and open fontanels. In this study, we found that Pin1, peptidyl prolyl cis-trans isomerase, is a critical regulator of Runx2 in vivo and in vitro. Pin1 mutant mice developed CCD-like phenotypes with hypoplastic clavicles and open fontanels as found in the Runx2+/- mice. In addition Runx2 protein level was significantly reduced in Pin1 mutant mice. Moreover Pin1 directly interacts with the Runx2 protein in a phosphorylation-dependent manner and subsequently stabilizes Runx2 protein. In the absence of Pin1, Runx2 is rapidly degraded by the ubiquitin-dependent protein degradation pathway. However, Pin1 overexpression strongly attenuated uniquitin-dependent Runx2 degradation. Collectively conformational change of Runx2 by Pin1 is essential for its protein stability and possibly enhances the level of active Runx2 in vivo.
机译：Runx2是主骨的转录因子形成。cleidocranial发育不良的遗传原因(CCD)特点是发育不全的锁骨和开放的囟门。Pin1,肽基prolyl顺反异构酶,是一个Runx2体内和体外的关键调节器。发达CCD-like Pin1突变小鼠表型发育不全的锁骨和开放囟门发现Runx2 + / -老鼠。蛋白质含量在Pin1显著降低突变的老鼠。Runx2的蛋白质中phosphorylation-dependent方式,随后稳定Runx2蛋白质。Runx2迅速退化的ubiquitin-dependent蛋白质降解途径。然而,Pin1过度强烈衰减uniquitin-dependent Runx2退化。集体Runx2的构象变化稳定和Pin1至关重要的蛋白质可能提高活性Runx2的水平活着。

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