This gene encodes a member of the ARID (AT-rich interaction domain) family of DNA binding proteins. It was found by homology to the Drosophila dead ringer gene, which is important for normal embryogenesis. Other ARID family members have roles in embryonic patterning, cell lineage gene regulation, cell cycle control, transcriptional regulation, and possibly in chromatin structure modification.[2]
↑Kortschak RD, Reimann H, Zimmer M, Eyre HJ, Saint R, Jenne DE (Jul 1998). "The human dead ringer/bright homolog, DRIL1: cDNA cloning, gene structure, and mapping to D19S886, a marker on 19p13.3 that is strictly linked to the Peutz-Jeghers syndrome". Genomics. 51 (2): 288–92. doi:10.1006/geno.1998.5259. PMID9722953.
↑Nixon JC, Rajaiya JB, Ayers N, Evetts S, Webb CF (Mar 2004). "The transcription factor, Bright, is not expressed in all human B lymphocyte subpopulations". Cellular Immunology. 228 (1): 42–53. doi:10.1016/j.cellimm.2004.03.004. PMID15203319.
↑Suzuki M, Okuyama S, Okamoto S, Shirasuna K, Nakajima T, Hachiya T, Nojima H, Sekiya S, Oda K (Aug 1998). "A novel E2F binding protein with Myc-type HLH motif stimulates E2F-dependent transcription by forming a heterodimer". Oncogene. 17 (7): 853–65. doi:10.1038/sj.onc.1202163. PMID9780002.
Further reading
Kortschak RD, Tucker PW, Saint R (Jun 2000). "ARID proteins come in from the desert". Trends in Biochemical Sciences. 25 (6): 294–9. doi:10.1016/S0968-0004(00)01597-8. PMID10838570.
Suzuki M, Okuyama S, Okamoto S, Shirasuna K, Nakajima T, Hachiya T, Nojima H, Sekiya S, Oda K (Aug 1998). "A novel E2F binding protein with Myc-type HLH motif stimulates E2F-dependent transcription by forming a heterodimer". Oncogene. 17 (7): 853–65. doi:10.1038/sj.onc.1202163. PMID9780002.
Peeper DS, Shvarts A, Brummelkamp T, Douma S, Koh EY, Daley GQ, Bernards R (Feb 2002). "A functional screen identifies hDRIL1 as an oncogene that rescues RAS-induced senescence". Nature Cell Biology. 4 (2): 148–53. doi:10.1038/ncb742. PMID11812999.
Kaiwen M (Jun 2002). "[Involvement of E2FBP1, an ARID family member protein, in the p53 regulatory pathway]". Kōkūbyō Gakkai Zasshi. the Journal of the Stomatological Society, Japan. 69 (2): 152–61. doi:10.5357/koubyou.69.152. PMID12136662.
Goebel P, Montalbano A, Ayers N, Kompfner E, Dickinson L, Webb CF, Feeney AJ (Sep 2002). "High frequency of matrix attachment regions and cut-like protein x/CCAAT-displacement protein and B cell regulator of IgH transcription binding sites flanking Ig V region genes". Journal of Immunology. 169 (5): 2477–87. doi:10.4049/jimmunol.169.5.2477. PMID12193717.
Ma K, Araki K, Ichwan SJ, Suganuma T, Tamamori-Adachi M, Ikeda MA (Apr 2003). "E2FBP1/DRIL1, an AT-rich interaction domain-family transcription factor, is regulated by p53". Molecular Cancer Research. 1 (6): 438–44. PMID12692263.
Fukuyo Y, Mogi K, Tsunematsu Y, Nakajima T (Jul 2004). "E2FBP1/hDril1 modulates cell growth through downregulation of promyelocytic leukemia bodies". Cell Death and Differentiation. 11 (7): 747–59. doi:10.1038/sj.cdd.4401412. PMID15017387.
Nixon JC, Rajaiya JB, Ayers N, Evetts S, Webb CF (Mar 2004). "The transcription factor, Bright, is not expressed in all human B lymphocyte subpopulations". Cellular Immunology. 228 (1): 42–53. doi:10.1016/j.cellimm.2004.03.004. PMID15203319.
Liao TT, Hsu WH, Ho CH, Hwang WL, Lan HY, Lo T, Chang CC, Tai SK, Yang MH (January 2016). "let-7 Modulates Chromatin Configuration and Target Gene Repression through Regulation of the ARID3B Complex". Cell Reports. 14 (3): 520–33. doi:10.1016/j.celrep.2015.12.064. PMID26776511. ARID3A was identified as let-7 target. Let-7i repressed ARID3A expression by binding to the 3′ UTR of the ARID3A transcript. In the absence of let-7, importin-9 facilitates the nuclear import of ARID3A, which then forms a complex with ARID3B.
