Negative feedback control of osteoclast formation through ubiquitin-mediated down-regulation of NFATc1

J Biol Chem. 2010 Feb 19;285(8):5224-31. doi: 10.1074/jbc.M109.042812. Epub 2009 Dec 26.

Abstract

The regulation of NFATc1 expression is important for osteoclast differentiation and function. Herein, we demonstrate that macrophage-colony-stimulating factor induces NFATc1 degradation via Cbl proteins in a Src kinase-dependent manner. NFATc1 proteins are ubiquitinated and rapidly degraded during late stage osteoclastogenesis, and this degradation is mediated by Cbl-b and c-Cbl ubiquitin ligases in a Src-dependent manner. In addition, NFATc1 interacts endogenously with c-Src, c-Cbl, and Cbl-b in osteoclasts. Overexpression of c-Src induces down-regulation of NFATc1, and depletion of Cbl proteins blocks NFATc1 degradation during late stage osteoclastogenesis. Taken together, our data provide a negative regulatory mechanism by which macrophage-colony-stimulating factor activates Src family kinases and Cbl proteins, and subsequently, induces NFATc1 degradation during osteoclast differentiation.

Publication types

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

MeSH terms

  • Animals
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology*
  • Cell Line
  • Down-Regulation / drug effects
  • Down-Regulation / physiology*
  • Humans
  • Macrophage Colony-Stimulating Factor / metabolism*
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Mice
  • Mice, Mutant Strains
  • NFATC Transcription Factors / metabolism*
  • Osteoclasts / metabolism*
  • Proto-Oncogene Proteins c-cbl / metabolism
  • Proto-Oncogene Proteins pp60(c-src) / metabolism
  • Ubiquitin / metabolism*

Substances

  • NFATC Transcription Factors
  • Nfatc1 protein, mouse
  • Ubiquitin
  • Macrophage Colony-Stimulating Factor
  • Proto-Oncogene Proteins c-cbl
  • Proto-Oncogene Proteins pp60(c-src)
  • Cbl protein, mouse