Genetic regulation of osteoclast development and function

By S. Teitelbaum, F. Ross. Nature reviews genetics, 2003

1,712 citations recorded by the source corpus.

Subfields: Molecular Biology, Nutrition and Dietetics, Oncology

View Paper: https://www.semanticscholar.org/paper/ce20a36fc9db01ee1a9d072e4bed63e2ebdb9d50

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. R. Jilka
2. Hiroshi Takayanagi
3. G. Karsenty
4. L. Xing
5. B. Boyce
6. S. Teitelbaum
7. Soo Young Lee
8. S. Manolagas

In Nutrition and Dietetics

1. B. Clarke
2. Hiroshi Takayanagi
3. G. Karsenty
4. L. Xing
5. B. Boyce
6. S. Teitelbaum

In Oncology

1. R. Jilka
2. G. Karsenty
3. S. Manolagas
4. Soo Young Lee
5. Hiroshi Takayanagi
6. N. Lee
7. B. Clarke
8. J. H. Park

Citations in the corpus

• Normal bone anatomy and physiology. (2008, background): “Both RANKL and M-CSF are produced mainly by marrow stromal cells and osteoblasts in membrane-bound and soluble forms, and osteoclastogenesis requires the presence of stromal cells and osteoblasts in bone marrow (28).”
• Current Understanding of RANK Signaling in Osteoclast Differentiation and Maturation (2017, background): “During the initiation step of RANK signaling, RANKL binding to RANK leads to the recruitment of adaptor proteins such as TRAF6 to the trimerized cytoplasmic tail of RANK and the rapid activation of MAPKs, NF-κB, and activator protein-1 (AP-1) (Kobayashi et al., 2001; Teitelbaum and Ross, 2003).”
• Matrix-embedded cells control osteoclast formation (2011, background): “Osteoclasts are multinucleated cells derived from the monocyte-macrophage lineage and are primarily responsible for resorption of mineralized matrice”
• 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].”
• Endocrine regulation of energy metabolism by the skeleton. (2007, background): “…of the two bone-specific cell types, 456 Cell 130, 456–469, August 10, 2007 ª2007 Elsevier Inc. osteoblasts and osteoclasts, are determined by secreted molecules that can either be cytokines acting locally or hormones acting systemically (Harada and Rodan, 2003; Teitelbaum and Ross, 2003).”
• Cancer to bone: a fatal attraction (2011, neutral): “RANKL binds to its cognate receptor, RANK, on osteoclast precursors, to induce osteoclastogenesis through the nuclear factor-κB (NF-κB), NFATc1 and JUN N-terminal kinase signalling pathway”
• Macrophages: development and tissue specialization. (2015, background): “osteoblast activity, result in skeletal pathologies, such as osteopetrosis or osteoporosis (155).”
• Leptin regulation of bone resorption by the sympathetic nervous system and CART (2005, methodology): “, osteoblasts increased expression of Rankl (a secreted osteoclast differentiation factor) to a greater extent than did parathyroid hormone (PTH), a hormone Figure 2 Sympathetic signalling in osteoblasts regulates BR. a,b, Osteoclast surface/ bone surface and Dpd/creatinine in 6-month-old mice; b, f”
• Insulin signaling in osteoblasts integrates bone remodeling and energy metabolism (2010, positive): “…and noticed that expression of Osteoprotegerin (Opg), a gene encoding a decoy receptor for RANKL and a negative regulator of osteoclast function (Teitelbaum and Ross, 2003), was increased 2-fold in InsR À/À and F H I G C 2 1 Expression relative to WT (fold) Opg 0.5 1.0 Expression relative to…”