Retinoblastoma protein-interacting zinc finger 1 (RIZ1) participates in RANKL-induced osteoclast formation via regulation of NFATc1 expression

Abstract The role of retinoblastoma protein-interacting zinc finger 1 (RIZ1) in receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation was examined in mouse RAW 264.7 macrophage-like cells. The expression of RIZ1 was significantly augmented by RANKL-treated cells. Silencing of RIZ1...

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Published inImmunology letters Vol. 131; no. 2; pp. 166 - 169
Main Authors Noman, Abu Shadat Mohammod, Koide, Naoki, Iftakhar-E-Khuda, Imtiaz, Dagvadorj, Jargalsaikhan, Tumurkhuu, Gantsetseg, Naiki, Yoshikazu, Komatsu, Takayuki, Yoshida, Tomoaki, Yokochi, Takashi
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 08.07.2010
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Summary:Abstract The role of retinoblastoma protein-interacting zinc finger 1 (RIZ1) in receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation was examined in mouse RAW 264.7 macrophage-like cells. The expression of RIZ1 was significantly augmented by RANKL-treated cells. Silencing of RIZ1 with the siRNA significantly reduced the appearance of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells as osteoclasts in RANKL-treated cells. The expression of nuclear factor of activated T cell 1 (NFATc1) as the terminal transcription factor of osteoclast formation was prevented by RIZ1 siRNA. It was suggested that that RIZ1 might participate in RANKL-induced osteoclast formation through the regulation of NFATc1 expression.
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ISSN:0165-2478
1879-0542
DOI:10.1016/j.imlet.2010.04.006