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TSH Is a Negative Regulator of Skeletal Remodeling
TLDR
A role for TSH is defined as a single molecular switch in the independent control of both bone formation and resorption in hyperthyroidism and osteoporosis.
Osteoclastic bone resorption by a polarized vacuolar proton pump.
TLDR
The mechanism by which osteoclasts transport protons into that resorptive microenvironment was identified by means of adenosine triphosphate-dependent weak base accumulation in isolated osteoclast membrane vesicles, which exhibited substrate and inhibition properties characteristic of the vacuolar, electrogenic H+-transporting H-ATPase.
Osteoclastogenesis, Bone Resorption, and Osteoclast‐Based Therapeutics
TLDR
This review focuses on key advances in understanding of molecular mechanisms underlying the formation, function, and survival of osteoclasts, including key signals mediating osteoclast differentiation, including PU.1, RANK, CSF‐1/c‐fms, and src.
FSH Directly Regulates Bone Mass
TLDR
It is suggested that high circulating FSH causes hypogonadal bone loss and that Osteoclasts and their precursors possess G(i2alpha)-coupled FSHRs that activate MEK/Erk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function.
Epidermal Growth Factor Activates m-Calpain (Calpain II), at Least in Part, by Extracellular Signal-Regulated Kinase-Mediated Phosphorylation
TLDR
Evidence is provided that m-calpain can be activated through the ERK cascade via direct phosphorylation and that this activation may occur in the absence of cytosolic calcium fluxes.
Glucocerebrosidase gene-deficient mouse recapitulates Gaucher disease displaying cellular and molecular dysregulation beyond the macrophage
TLDR
Direct evidence is provided for the involvement in GD1 of multiple cell lineages, suggesting that cells other than macrophages may be worthwhile therapeutic targets.
Epidermal Growth Factor as a Candidate for Ex Vivo Expansion of Bone Marrow–Derived Mesenchymal Stem Cells
TLDR
Findings suggest that EGFR ligands could be used for ex vivo expansion and direction of BMMSCs, and that PDGF did interfere with the differentiation of these BMMSC lineages.
PINCH-1 Regulates the ERK-Bim Pathway and Contributes to Apoptosis Resistance in Cancer Cells*
TLDR
A strong dependence of multiple types of apoptosis-resistant cancer cells on PINCH-1 is demonstrated and new insights are provided into the molecular mechanism by which cancer cells are protected from apoptosis.
Parathyroid Hormone Receptor Directly Interacts with Dishevelled to Regulate β-Catenin Signaling and Osteoclastogenesis*
TLDR
It is reported that the PTH1R activates the β-catenin pathway by directly recruiting Dvl, independent of Wnt or LRP5/6, and demonstrates that G protein-coupled receptors other than FZD directly activate β-catsin signaling, thereby mimicking many of the functions of the canonical Wnt-FZD pathway.
Follicle-stimulating hormone stimulates TNF production from immune cells to enhance osteoblast and osteoclast formation
TLDR
It is proposed that hypogonadal bone loss is caused, at least in part, by enhanced FSH secretion, which in turn increases TNFα production to expand the number of bone marrow osteoclast precursors.
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