Doubly truncated FosB isoform (Delta2DeltaFosB) induces osteosclerosis in transgenic mice and modulates expression and phosphorylation of Smads in osteoblasts independent of intrinsic AP-1 activity.

@article{Sabatakos2008DoublyTF,
  title={Doubly truncated FosB isoform (Delta2DeltaFosB) induces osteosclerosis in transgenic mice and modulates expression and phosphorylation of Smads in osteoblasts independent of intrinsic AP-1 activity.},
  author={George Sabatakos and Glenn C Rowe and Marie Kveiborg and Meilin Wu and L. Neff and Riccardo Chiusaroli and William M. Philbrick and Roland Baron},
  journal={Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research},
  year={2008},
  volume={23 5},
  pages={584-95}
}
INTRODUCTION Activator protein (AP)-1 family members play important roles in the development and maintenance of the adult skeleton. Transgenic mice that overexpress the naturally occurring DeltaFosB splice variant of FosB develop severe osteosclerosis. Translation of Deltafosb mRNA produces both DeltaFosB and a further truncated isoform (Delta2DeltaFosB) that lacks known transactivation domains but, like DeltaFosB, induces increased expression of osteoblast marker genes. MATERIALS AND METHODS… CONTINUE READING
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