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노아롱새미(A Long Saemi Noh),임미정(Mijung Yim) 대한약학회 2010 약학회지 Vol.54 No.6
We investigated the role of L-type Ca2+ channel in receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast formation. BayK 8644, a L-type Ca2+ channel agonist, was shown to increase the RANKLinduced osteoclastogenesis and actin ring formation in mouse bone marrow-dereived macrophage (BMM) culture system. BayK 8644 stimulated RANKL-induced extracellular signal-regulated kinase (ERK) and p38 MAP kinase (MAPK) activation, which leads to increased nuclear factor of activated T cells (NFAT)c1 expression. Taken together, these data indicate that L-type Ca2+ channel regulates osteoclast formation possibly through ERK- and p38-mediated NFATc1 expression.
박효정(Hyojung Park),노아롱새미(A Long Saemi Noh),이정민(Jung-Min Lee),임미정(Mijung Yim) 대한약학회 2010 약학회지 Vol.54 No.5
We explored the role of phosphodiesterase 4 (PDE4) on parathyroid (PTH)-induced signaling in osteoblasts. PTH was shown to increase the activity of PDE, mainly PDE4, in osteoblasts, which is partly attributable to elevated PDE4B and PDE4D mRNA expression. The use of PDE4 inhibitor strengthened the PTH-induced extracellular signal-regulated kinase (ERK) and p38 MAP kinase (MAPK) activation. Furthermore, the PDE4 inhibitor stimulated PTH-induced receptor activator of nuclear factor-κB ligand (RANKL) expression in osteoblasts, which in turn increased osteoclast formation. Taken together, these data suggest the negative role of PDE4 on PTH-induced signaling in osteoblasts.