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NOTCH1 Regulates Osteoclastogenesis Directly in Osteoclast Precursors and Indirectly via Osteoblast Lineage Cells*
TLDR
It is found that attenuated Notch signaling enhances osteoclastogenesis and bone resorption in vitro and in vivo by a combination of molecular mechanisms, and raises caution that therapeutic inhibition of NOTCH signaling may adversely accelerate bone loss in humans.
Syk, c-Src, the αvβ3 integrin, and ITAM immunoreceptors, in concert, regulate osteoclastic bone resorption
TLDR
In conjunction with ITAM-bearing proteins, Syk, c-Src, and αvβ3 represent an essential signaling complex in the bone-resorbing osteoclast, and, therefore, each is a candidate therapeutic target.
Rac deletion in osteoclasts causes severe osteopetrosis
TLDR
The dysfunction of RacDKO osteoclasts represents failed cytoskeleton organization as evidenced by reduced motility of the cells and their inability to spread or generate the key resorptive organelles, which is accompanied by abnormal Arp3 distribution.
Syk, c-Src, the alphavbeta3 integrin, and ITAM immunoreceptors, in concert, regulate osteoclastic bone resorption.
TLDR
In conjunction with ITAM-bearing proteins, Syk, c-Src, and alpha v beta3 represent an essential signaling complex in the bone-resorbing osteoclast, and, therefore, each is a candidate therapeutic target.
c-Jun NH2-Terminal Kinase-Mediated Up-regulation of Death Receptor 5 Contributes to Induction of Apoptosis by the Novel Synthetic Triterpenoid Methyl-2-Cyano-3,12-Dioxooleana-1, 9-Dien-28-Oate in
TLDR
It is concluded that CDDO-Me induces apoptosis via the JNK-mediated DR up-regulation in human lung cancer cells through a p53-independent mechanism.
Cdc42 regulates bone modeling and remodeling in mice by modulating RANKL/M-CSF signaling and osteoclast polarization.
TLDR
It is demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation of Rb and induced caspase 3 and Bim, thus contributing to osteoclast proliferation and apoptosis rates, and was a component of the Par3/Par6/atypical PKC polarization complex in osteoclasts.
The ADP receptor P2RY12 regulates osteoclast function and pathologic bone remodeling.
TLDR
It is demonstrated that P2RY12 is the primary ADP receptor in OCs and suggest that P1RY12 inhibition is a potential therapeutic target for pathologic bone loss.
CpG Oligodeoxynucleotides Modulate the Osteoclastogenic Activity of Osteoblasts via Toll-like Receptor 9*
TLDR
CpG ODN activity (modulation of osteoclastogenesis, gene expression, ERK and p38 phosphorylation, and nuclear translocation of NFκB) is specific, because the control oligodeoxynucleotide, not containing CpG, is inactive.
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