Overexpression of ΔFosB transcription factor(s) increases bone formation and inhibits adipogenesis

@article{Sabatakos2000OverexpressionO,
  title={Overexpression of $\Delta$FosB transcription factor(s) increases bone formation and inhibits adipogenesis},
  author={George Sabatakos and Natalie A. Sims and J. Chen and Kazuhiro Aoki and Max B Kelz and Michael Amling and Yasmina Bouali and Keya De Mukhopadhyay and Kl Ford and Eric J. Nestler and Roland Baron},
  journal={Nature Medicine},
  year={2000},
  volume={6},
  pages={985-990}
}
Members of the AP-1 family of transcription factors participate in the regulation of bone cell proliferation and differentiation. We report here a potent AP-1-related regulator of osteoblast function: ΔFosB, a naturally occurring truncated form of FosB that arises from alternative splicing of the fosB transcript and is expressed in osteoblasts. Overexpression of ΔFosB in transgenic mice leads to increased bone formation throughout the skeleton and a continuous post-developmental increase in… 
Transcription factors controlling osteoblastogenesis.
  • P. Marie
  • Biology
    Archives of biochemistry and biophysics
  • 2008
ΔFosB Induces Osteosclerosis and Decreases Adipogenesis by Two Independent Cell-Autonomous Mechanisms
TLDR
It is concluded that the changes in osteoblast and adipocyte differentiation in ΔFosB transgenic mice result from independent cell-autonomous mechanisms.
A CCAAT/Enhancer Binding Protein β Isoform, Liver-Enriched Inhibitory Protein, Regulates Commitment of Osteoblasts and Adipocytes
TLDR
Interestingly, an isoform of C/EBPβ, liver-enriched inhibitory protein (LIP), which lacks the transcriptional activation domain, stimulates transcriptional activity and the osteogenic action of Runx2, although LIP inhibits adipogenesis in a dominant-negative fashion.
Control of Bone Formation by AP-1 Transcription Factor and Rho GTPases: Implications for Bone Regeneration and Tissue Repair
TLDR
It is shown that Rho activation inhibits calvarial osteogenic cell differentiation and bone formation in vitro, while treatment of osteogenic cultures with ROCK inhibitors gives an anabolic response, markedly stimulating bone formation.
Ebf1-dependent control of the osteoblast and adipocyte lineages.
Doubly Truncated FosB Isoform (Δ2ΔFosB) Induces Osteosclerosis in Transgenic Mice and Modulates Expression and Phosphorylation of Smads in Osteoblasts Independent of Intrinsic AP‐1 Activity
  • G. Sabatakos, G. Rowe, R. Baron
  • Biology
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2008
TLDR
Transgenic mice that overexpress the naturally occurring ΔFosB splice variant of FosB develop severe osteosclerosis, and translation of Δfosb mRNA produces a further truncated isoform that lacks known transactivation domains but induces increased expression of osteoblast marker genes.
Role of menin in bone development.
TLDR
In mature osteoblasts the interaction of menin and the TGF-beta/ Smad3 pathway counteracts the BMP-2/Smad1/5- and Runx2-induced transcriptional activities leading to inhibition of late stage osteoblast differentiation.
Zinc Finger Protein 467 Is a Novel Regulator of Osteoblast and Adipocyte Commitment*
TLDR
Zfp467 is a novel co-factor that promotes adipocyte differentiation and suppresses osteoblast differentiation and has relevance to therapeutic interventions in osteoporosis, including PTH-based therapies currently available, and may be of relevance for the use of adipose-derived stem cells for tissue engineering.
Elevated Fra-1 expression causes severe lipodystrophy
TLDR
To the known common systemic control of fat and bone mass, a new cell-autonomous level of control of cell fate decision by which the osteogenic transcription factor Fra-1 opposes adipocyte differentiation by inhibiting C/EBPα is added.
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