Canonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytes.
By Theo P. Hill, Daniela Später, M. Taketo, W. Birchmeier, C. Hartmann. Developmental Cell, 2005
1,141 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/34b606c4cd92f3ec981e2fa92cff609b3032451d
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In Genetics
- T. Komori
- Fanxin Long
- Christopher S. Chen
- Andrew P. McMahon
- M. Goldring
- D. Ornitz
- S. Angers
- W. Birchmeier
In Molecular Biology
- T. Komori
- Fanxin Long
- D. Ornitz
- Christopher S. Chen
- E. Eriksen
- Andrew P. McMahon
- M. Goldring
- S. Angers
Citations in the corpus
- Regulation of osteoblast differentiation by transcription factors (2006, background): “Finally, conditional deletion of b-catenin gene in Dermo-Cre or Prx1-Cre transgenicmice revealed an essential role of b-catenin in osteoblast differentiation [Day et al., 2005; Hill et al., 2005; Hu et al., 2005].”
- Activation of β-Catenin Signaling in Articular Chondrocytes Leads to Osteoarthritis-Like Phenotype in Adult β-Catenin Conditional Activation Mice (2008, background): “Conditional deletion of the -catenin gene in early mesenchymal progenitor cells (targeted by Prx1-Cre or Dermo1-Cre) results in enhanced chondrogenesis,((6,7)) suggesting that -catenin inhibits early mesenchymal cell differentiation into chondrocytes.”
- Cellular mechanisms of bone remodeling (2010, background): “Canonical Wnt signaling in osteoblast differentiation is modulated by Runx2 and osterix [21].”
- Multiple roles of mesenchymal β-catenin during murine limb patterning (2006, methodology): “S4 in the supplementary material) (Hill et al., 2005).”
- Mechanical control of stem cell differentiation (2008, background): “β-catenin, in particular, appears to promote a chondro-to-osteo differentiation switch in progenitor cells/mesenchymal stem cells (Day et al., 2005; Hill et al., 2005).”
- Development of the endochondral skeleton. (2013, background): “Interestingly, deletion of b-catenin in either mesenchymal progenitors or OSX-positive cells caused ectopic cartilage formation in place of bone, possibly owing to a fate switch for the bipotential progenitors (Day et al. 2005; Hill et al. 2005; Hilton et al. 2005; Rodda and McMahon 2006).”
- Regulation of Proliferation, Differentiation and Functions of Osteoblasts by Runx2 (2019, background): “Conditional Ctnnb1 knockout mice created by crossing with Col2a1 promoter Cre transgenic mice or Prrx1 promoter Cre transgenic mice in which Ctnnb1 is deleted in osteoblast progenitors in calvaria and osteo-chondroprogenitors in limb skeletons also lack osteoblasts in the Cre-expressing skeletons [1”
- Distinct roles for Hedgehog and canonical Wnt signaling in specification, differentiation and maintenance of osteoblast progenitors (2006, background): “Bmps are implicated in the specification of both chondrocytes and osteoblasts (reviewed by Hoffmann and Gross, 2001), as well as in the subsequent modification of the osteogenic program, where some Bmps promote bone formation [such as Bmp2, Bmp7, Bmp6 and Bmp9 (Peng et al., 2003)], although Bmp3…”
- The control of chondrogenesis (2006, background): “…pathway and activation of TCF/Lef transcription factors, functions in a cell autonomous manner to induce osteoblast differentiation and suppress chondrocyte differentiation in early chondroprogenitors [Day et al., 2005; Gaur et al., 2005; Glass et al., 2005; Hill et al., 2005; Hu et al., 2005].”