Simon W. Fox
University of Plymouth
34 Papers
488 Citations
Simon W. Fox is an academic researcher from University of Plymouth. The author has contributed to research in topics: Osteoclast & RANKL. The author has an hindex of 25, co-authored 33 publications. Previous affiliations of Simon W. Fox include Howard Hughes Medical Institute & St George's Hospital.
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Papers
TRANCE Is Necessary and Sufficient for Osteoblast-mediated Activation of Bone Resorption in Osteoclasts
TL;DR: TRANCE expression by osteoblasts appears to be both necessary and sufficient for hormone-mediated activation of mature osteoclasts, and TRANCE-R is likely to be a receptor for signal transduction for activation of the osteoclast and its survival.
Nitric oxide is an early mediator of the increase in bone formation by mechanical stimulation
TL;DR: The ability of NG-monomethyl-L-arginine, an inhibitor of NO synthase (NOS), to suppress the osteogenic response in a recently developed model of mechanically induced osteogenesis suggests that early release of NO is a key signal in the transduction of mechanical stimuli into subsequent bone formation.
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Interleukin-10 inhibits osteoclastogenesis by reducing NFATc1 expression and preventing its translocation to the nucleus.
Kathryn E Evans,Simon W. Fox +1 more
TL;DR: This is the first report indicating that one of the ways in which IL-10 directly inhibits osteoclastogenesis is by suppressing NFATc1 activity, and provides evidence that the mechanism may involve disruption of Ca2+ mobilisation.
Role of Nitric Oxide and Prostaglandins in Mechanically Induced Bone Formation
TL;DR: It is found that while exogenous NO potentiates the stimulatory effect of mechanical loading on bone formation, the lack of effect in nonloaded vertebrae suggests that NO is necessary but not sufficient for induction of bone formation.
133
Role for parathyroid hormone in mechanical responsiveness of rat bone
TL;DR: A major role for PTH is revealed in the mechanical responsiveness of rat bone by sensitizing either the strain-sensing mechanism itself or early responses of bone to strain-generated signals.
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