Post-translational Regulation of Runx2 in Bone and Cartilage

J Dent Res. 2009 Aug;88(8):693-703. doi: 10.1177/0022034509341629.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Acetylation
  • Bone Development / genetics
  • Bone and Bones / metabolism*
  • Cartilage / metabolism*
  • Chondrocytes / metabolism
  • Core Binding Factor Alpha 1 Subunit / genetics*
  • Humans
  • Odontogenesis / genetics
  • Osteoblasts / metabolism
  • Phosphorylation
  • Protein Biosynthesis / genetics
  • Protein Processing, Post-Translational / genetics*
  • Transcription, Genetic / genetics
  • Ubiquitination

Substances

  • Core Binding Factor Alpha 1 Subunit
  • RUNX2 protein, human