Therapeutic approaches to bone diseases.

By G. Rodan, T. Martin. Science, 2000

1,745 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine

View Paper: https://www.semanticscholar.org/paper/c633ebb37ee4d628f27422f677a90fbde9439f86

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In Molecular Biology

In Oncology

In Orthopedics and Sports Medicine

Citations in the corpus

RANKL maintains bone homeostasis through c-Fos-dependent induction of interferon-β (2002, background): “jpg" NDATA ITEM> ]> Osteoclasts are cells of monocyte/macrophage origin that erode bone matrix: regulation of their differentiation is central to the understanding of the pathogenesis and treatment of bone diseases such as osteoporosis”
Bone dysplasia sclerosteosis results from loss of the SOST gene product, a novel cystine knot-containing protein. (2001, background): “Currently there is no effective treatment for the restoration of normal bone mass in individuals with pathologically low skeletal density, and there is a large unmet need for therapy that can increase bone deposition in osteoporosis (Rodan and Martin 2000).”
Control of osteoblast function and regulation of bone mass (2003, background): “There are, however, examples in bone diseases where these requirements could be me”
Osteoclast differentiation and activation (2003, background): “Most adult skeletal diseases are due to excess osteoclastic activity, leading to an imbalance in bone remodelling which favours resorptio”
Calcium Orthophosphates in Nature, Biology and Medicine (2009, background): “Unlike other mineralized tissues, bone continuously undergoes a remodeling process, as it is resorbed by specialized cells called osteoclasts and formed by another type of cells called osteoblasts (so called “bone lining cells”) in a delicate equilibrium [353,393,396,437,438].”
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”
Endocrine regulation of male fertility by the skeleton. (2011, positive): “The biological importance of this regulation is best exemplified by the fact that gonadal failure triggers bone loss and causes osteoporosis in postmenopausal women (Manolagas et al., 2002; Rodan and Martin, 2000).”
Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. (2000, background): “Syk is also negatively regulated by the ubiquitinating activity of cCbl (50;51).”