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Hideki Kitaura

Researcher at Tohoku University

Publications -  112
Citations -  5374

Hideki Kitaura is an academic researcher from Tohoku University. The author has contributed to research in topics: Osteoclast & Bone resorption. The author has an hindex of 32, co-authored 102 publications receiving 4668 citations. Previous affiliations of Hideki Kitaura include Nagasaki University & Washington University in St. Louis.

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IL-1 mediates TNF-induced osteoclastogenesis

TL;DR: IL-1 mediates the osteoclastogenic effect of TNF by enhancing stromal cell expression of RANKL and directly stimulating differentiation of osteoclass precursors under the aegis of p38 MAPK.
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Glucocorticoids suppress bone formation via the osteoclast

TL;DR: Compared with osteoclasts modulating the osteoblast-suppressive effect of DEX, GRoc-/- mice are protected from the steroid's inhibition of bone formation, suggesting that an intermediary cell transmits a component of the bone-suppression effects of GCs to osteoblasts in the intact animal.
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U0126 and PD98059, specific inhibitors of MEK, accelerate differentiation of RAW264.7 cells into osteoclast-like cells.

TL;DR: It is suggested that osteoclastogenesis is regulated under a balance between ERK and p38 pathways and that the MEK/ERK pathway negatively regulates osteoclineogenesis while the p38 pathway does so positively.
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M-CSF mediates TNF-induced inflammatory osteolysis

TL;DR: Confirming that inhibition of the M-CSF signaling pathway targets TNF-alpha, anti-c-Fms also completely arrested osteolysis in T NF-injected mice with nominal effect on macrophage number, presenting as candidate therapeutic targets in states of inflammatory bone erosion.
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Syk, c-Src, the αvβ3 integrin, and ITAM immunoreceptors, in concert, regulate osteoclastic bone resorption

TL;DR: 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.