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

Abu Shadat Mohammod Noman, Naoki Koide, Imtiaz Iftakhar-E-Khuda, Jargalsaikhan Dagvadorj, Gantsetseg Tumurkhuu, Yoshikazu Naiki, Takayuki Komatsu, Tomoaki Yoshida, Takashi Yokochi

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10 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)166-169
Number of pages4
JournalImmunology Letters
Volume131
Issue number2
DOIs
Publication statusPublished - 07-2010

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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