Post-translational Regulation of Runx2 in Bone and Cartilage.
Post-translational Regulation of Runx2 in Bone and Cartilage.
复制标题
DOI：
10.1177/0022034509341629
复制
发表时间：
2009-08
影响因子：
7.6
通讯作者：
Chen D
中科院分区：
文献类型：
--
作者：
Jonason JH;Xiao G;Zhang M;Xing L;Chen D
Runx 2基因产物是哺乳动物骨骼发育所必需的。在人类中，Runx 2单倍不足导致锁骨颅骨发育不良，这是一种以骨和牙齿异常为特征的骨骼疾病。在分子水平上，Runx 2作为在肥大软骨细胞和成骨细胞中表达的基因的转录因子。Runx 2基因表达和蛋白质功能在多个水平上受到调控，包括转录、翻译和翻译后修饰。此外，Runx 2参与许多蛋白质-蛋白质相互作用，其中大多数激活或抑制靶基因的转录。在这篇综述中，我们讨论了Runx 2在发育过程中的表达，以及通过磷酸化，泛素化和乙酰化修饰的Runx 2的翻译后调节。
The Runx2 gene product is essential for mammalian bone development. In humans, Runx2 haploinsufficiency results in cleidocranial dysplasia, a skeletal disorder characterized by bone and dental abnormalities. At the molecular level, Runx2 acts as a transcription factor for genes expressed in hypertrophic chondrocytes and osteoblasts. Runx2 gene expression and protein function are regulated on multiple levels, including transcription, translation, and post-translational modification. Furthermore, Runx2 is involved in numerous protein-protein interactions, most of which either activate or repress transcription of target genes. In this review, we discuss expression of Runx2 during development as well as the post-translational regulation of Runx2 through modification by phosphorylation, ubiquitination, and acetylation.