title: Critical role of ARID3B in the expression of pro-apoptotic p53-target genes and apoptosis.
abstract: ARID3A and ARID3B are transcriptional targets of p53. Recently, it has been reported that ARID3A plays a critical role in the transcriptional activation of pro-arrest p21 in response to DNA damage. However, the role of ARID3B in the p53 regulatory pathway remains poorly understood. Here we show that ARID3A and ARID3B specifically bind to putative ARID3-binding sites in p53 target genes in vitro and in vivo. ARID3B and, to a lesser extent, ARID3A silencing blocked transcriptional activation of pro-apoptotic p53 target genes, such as PUMA, PIG3, and p53. Furthermore, ectopic ARID3B, to a lesser extent, ARID3A expression activated the pro-apoptotic gene expression, and only ARID3B induced apoptosis. Finally, ARID3B but not ARID3A silencing blocked apoptosis induction following DNA damage. These results indicated that, although ARID3B and ARID3A share overlapping functions, ARID3B play a key role in the expression of pro-apoptotic p53-target genes and apoptosis.
authors.affiliation: Department of Molecular Craniofacial Embryology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Endrawan
authors.initials: E
authors.lastname: Pratama
authors.affiliation: Department of Oral Implantology and Regenerative Dental Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Tian
authors.affiliation: Faculty of Dentistry, International Islamic University Malaysia, Kuantan, Malaysia.
authors.forename: Widya
authors.initials: W
authors.lastname: Lestari
authors.affiliation: Department of Molecular Craniofacial Embryology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Sachiko
authors.initials: S
authors.lastname: Iseki
authors.affiliation: Faculty of Dentistry, International Islamic University Malaysia, Kuantan, Malaysia.
authors.forename: Solachuddin J A
authors.initials: SJ
authors.lastname: Ichwan
authors.affiliation: Department of Molecular Craniofacial Embryology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan. Electronic address: mikeda.emb@tmd.ac.jp.
authors.forename: Masa-Aki
authors.initials: MA
authors.lastname: Ikeda
mesh_terms: D017209:Apoptosis; D045744:Cell Line, Tumor; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics; D004249:DNA Damage; D004268:DNA-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D005786:Gene Expression Regulation; D020868:Gene Silencing; D006801:Humans; D011401:Promoter Regions, Genetic; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D015533:Transcriptional Activation; D016159:Tumor Suppressor Protein p53 / Q000235:genetics* / Q000378:metabolism
chemical_list: C490798:ARID3A protein, human; C120893:ARID3B protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004268:DNA-Binding Proteins; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53
keywords: ARID3A; ARID3B; Apoptosis; Gene expression; p53