title: 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-kappaB 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.
authors.affiliation: Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan.
authors.forename: Abu Shadat Mohammod
authors.initials: AS
authors.lastname: Noman
authors.forename: Naoki
authors.initials: N
authors.lastname: Koide
authors.forename: Imtiaz
authors.initials: I
authors.lastname: Iftakhar-E-Khuda
authors.forename: Jargalsaikhan
authors.initials: J
authors.lastname: Dagvadorj
authors.forename: Gantsetseg
authors.initials: G
authors.lastname: Tumurkhuu
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Naiki
authors.forename: Takayuki
authors.initials: T
authors.lastname: Komatsu
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Yoshida
authors.forename: Takashi
authors.initials: T
authors.lastname: Yokochi
mesh_terms: D000135:Acid Phosphatase / Q000096:biosynthesis; D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis; D001862:Bone Resorption; D002460:Cell Line; D005786:Gene Expression Regulation; D011495:Histone-Lysine N-Methyltransferase / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D007527:Isoenzymes / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D050778:NFATC Transcription Factors / Q000096:biosynthesis* / Q000235:genetics; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D010010:Osteoclasts / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D053245:RANK Ligand / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D000071681:Tartrate-Resistant Acid Phosphatase; D014157:Transcription Factors / Q000235:genetics / Q000276:immunology / Q000378:metabolism*
chemical_list: D000943:Antigens, Differentiation; D007527:Isoenzymes; D050778:NFATC Transcription Factors; D053245:RANK Ligand; D034741:RNA, Small Interfering; C505689:Tnfsf11 protein, mouse; D014157:Transcription Factors; D011495:Histone-Lysine N-Methyltransferase; C489242:Prdm2 protein, mouse; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase