Reaching a genetic and molecular understanding of skeletal development.

By G. Karsenty, E. Wagner. Developmental Cell, 2002

1,431 citations recorded by the source corpus.

In the last ten years, we have made considerable progress in our genetic and molecular understanding of all aspects of skeletal development, chondrogenesis, joint formation, and osteogenesis. This review addresses the role of the principal growth factors and transcription factors affecting these different processes and presents, in several cases, the genetic cascade leading to cell differentiation.

Subfields: Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e3a4d37f7cd92f101598d4f0f49819a70b576ad6

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In Genetics

1. Fanxin Long
2. H. Kronenberg
3. P. Marie
4. D. Ornitz
5. Hiroshi Takayanagi
6. L. Xing
7. B. Boyce
8. M. Zaidi

In Molecular Biology

1. Fanxin Long
2. S. Teitelbaum
3. Hiroshi Takayanagi
4. D. Ornitz
5. L. Xing
6. B. Boyce
7. E. Olson
8. G. Karsenty

Citations in the corpus

• Bone-marrow haematopoietic-stem-cell niches (2006, background): “In this respect, several other mouse mutants with defects in bone development and/or remodelling have been describe”
• Bidirectional ephrinB2-EphB4 signaling controls bone homeostasis. (2006, background): “Bone-resorbing osteoclasts are large, multinucleated cells derived from monocyte-macrophage precursors, while bone-forming osteoblasts are derived from mesenchymal cells (Karsenty and Wagner, 2002; Teitelbaum and Ross, 2003).”
• Notch signaling maintains bone marrow mesenchymal progenitors by suppressing osteoblast differentiation (2008, background): “Because osteoblasts are known to balance osteoclastogenesis through production of the positive regulator RANKL (encoded by Tnfsf11 ) and the antagonist osteoprotegerin (encoded by Tnfrsf11b”
• TSH is a negative regulator of skeletal remodeling. (2003, background): “This makes more dephosphorylated I B available to bind to and hence prevent the nuclear translocation less clear on the mechanism through which Flk-1 mediates TSH effects on osteoblastogenesis, except thatof NF B heterodimers.”
• Transforming Growth Factor- 1 to the Bone (2005, background): “Local growth factors and cytokines regulating osteoblast differentiation include BMPs, fibroblast growth factors, platelet-derived growth factor (PDGF), IGFs, and Indian Hedgehog (103).”
• A twist code determines the onset of osteoblast differentiation. (2004, neutral): “identification of genes regulating it specifically (Karsenty and Wagner, 2002).”
• Control of osteoblast function and regulation of bone mass (2003, background): “Based on skeletal phenotype associated with genetic mutations in animals and humans and the analysis of transcriptional complexes formed with osteoblast/chondrocyte-specific enhancers, a number of transcription factors that control osteogenesis and chondrogenesis have been identifie”
• Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis (2004, background): “The development and homeostasis of the skeletal system depend on the balance between bone formation and resorptio”
• Conditional inactivation of FGF receptor 2 reveals an essential role for FGF signaling in the regulation of osteoblast function and bone growth (2003, background): “The Indian hedgehog (IHH) signaling pathway is an important regulator of chondrocyte proliferation and differentiation (Karsenty and Wagner, 2002; Ornitz and Fig.”
• ATF4 is a substrate of RSK2 and an essential regulator of osteoblast biology; implication for Coffin-Lowry Syndrome. (2004, neutral): “Histomor- leucine zipper proteins as well as Runx2 and Osterix, two transcription factors necessary for osteoblast differ-phometric analysis established that the bone formation rate (BFR), an indicator of osteoblast function, and the entiation (Karsenty and Wagner, 2002).”
• Effect of DHA content in rotifers on the occurrence of skeletal deformities in red porgy Pagrus pagrus (Linnaeus, 1758) (2009, background): “Moreover, expression of osteogenic markers related to the occurrence of skeletal abnormalities, such as OC and MGPC (Karsenty and Wagner, 2002), seem to be affected by the presence of essential fatty acids (Pombinho et al.”
• Biology of RANK, RANKL, and osteoprotegerin (2007, background): “Indeed, the development of osteopetrosis in a variety of knockout mice has identified necessary functions of genes in osteoclast biology that largely had not been anticipated [3,4].”
• Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation (2017, background): “Osteoclasts are bone-resorbing multinucleated cells that originate from hematopoietic precursors that are formed in the bone marrow (Asagiri and Takayanagi, 2007; Boyle et al., 2003; Karsenty and Wagner, 2002; Teitelbaum, 2000).”