Distinct roles for Hedgehog and canonical Wnt signaling in specification, differentiation and maintenance of osteoblast progenitors

By Stephen J. Rodda, Andrew P. McMahon. Development, 2006

1,025 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c526709b145e97e7bd85c542e7ea7c7a0f3d7eb8

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In Molecular Biology

Citations in the corpus

Endogenous Bone Marrow MSCs Are Dynamic, Fate-Restricted Participants in Bone Maintenance and Regeneration (2012, background): “Osterix (Osx) is known to be expressed earlier than osteocalcin in the osteoblast lineage (Rodda and McMahon, 2006).”
Osteoblast Precursors, but Not Mature Osteoblasts, Move into Developing and Fractured Bones along with Invading Blood Vessels (2010, neutral): “Osx-Cre:GFP mice have been described (Rodda and McMahon, 2006).”
From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “naling increases (94, 95, 279, 280) whereas Alox15 and”
Matrix-embedded cells control osteoclast formation (2011, methodology): “Medium was completely changed at days 8 and 10 and at day 10, the cells were treated with vehicle or 10-7 M human PTH (1–34) for 4 hours before RNA extraction.”
Molecular and cellular mechanisms of the anabolic effect of intermittent PTH. (2007, background): “The replication, differentiation and survival of osteoblast progenitors is controlled by locally produced autocrine/paracrine factors including members of the Wnt, Hedgehog and bone morphogenetic protein (BMP) families, as well as transforming growth factor-β (TGF-β), insulin-like growth factor-I (I”
Six2 defines and regulates a multipotent self-renewing nephron progenitor population throughout mammalian kidney development (2008, background): “The TGC alleles were designed to enable doxycycline-regulated control of an eGFPCre transgene within the Six2 expression domain (Bond et al., 2000; 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”