Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis.

By T. Day, Xizhi Guo, L. Garrett-Beal, Yingzi Yang. Developmental Cell, 2005

1,691 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d2cd522e49842fe79cf880a980b3b8b14a2da13d

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Citations in the corpus

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 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].”
Wnt signaling in development and tissue homeostasis (2018, background): “The precise roles of Wnt-β -catenin signaling in bone mass homeostasis still remain to be clarified but the prevailing model is that it functions to regulate osteoblast differentiation and function (Bennett et al., 2005; Cui et al., 2011; Day et al., 2005; Hill et al., 2005; Tu et al., 2015).”
Multiple roles of mesenchymal β-catenin during murine limb patterning (2006, background): “Lack of -catenin does not inhibit chondrocyte differentiation, on the contrary it stimulates it (Day et al., 2005; Hill et al., 2005).”
Regulation of Proliferation, Differentiation and Functions of Osteoblasts by Runx2 (2019, background): “In conditional Ctnnb1 knockout mice created by crossing with Twist2 (Dermo1) Cre knock-in mice in which Ctnnb1 is deleted in osteo-chondroprogenitors, osteoblasts are absent, Runx2 is expressed in the perichondrial cells, and Sp7 expression is weak or absent in perichondrial cells [27,28].”
Distinct roles for Hedgehog and canonical Wnt signaling in specification, differentiation and maintenance of osteoblast progenitors (2006, methodology): “, 2005) (data not shown), and Wnt signaling is itself implicated in the chondrogenic program (Day 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).”
Activation of β-Catenin Signaling in Articular Chondrocytes Leads to Osteoarthritis-Like Phenotype in Adult β-Catenin Conditional Activation Mice (2008, background): “Chondrocyte maturation is accelerated in these mice but occurs in the setting of severe chondrodysplasia.((7,8)) Exon 3 of the -catenin gene encodes for the serine and threonine residues that are phosphorylated by GSK-3 and targeted by protein degradation mechanism.”
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].”