ARID3A

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
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AT-rich interactive domain-containing protein 3A is a protein that in humans is encoded by the ARID3A gene.[1][2]

Function

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]

Interactions

ARID3A has been shown to interact with:

References

  1. 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. PMID 9722953.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  2. 2.0 2.1 "Entrez Gene: ARID3A AT rich interactive domain 3A (BRIGHT-like)".<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  3. 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. PMID 15203319.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  4. 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. PMID 9780002.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>

Further reading

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  • 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. PMID 10838570.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 9780002.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 11812999.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 12136662.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 12193717.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 12692263.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 15017387.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 15203319.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Rajaiya J, Nixon JC, Ayers N, Desgranges ZP, Roy AL, Webb CF (Jun 2006). "Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I". Molecular and Cellular Biology. 26 (12): 4758–68. doi:10.1128/MCB.02009-05. PMC 1489113. PMID 16738337.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Olsen JV, Blagoev B, Gnad F, Macek B, Kumar C, Mortensen P, Mann M (Nov 2006). "Global, in vivo, and site-specific phosphorylation dynamics in signaling networks". Cell. 127 (3): 635–48. doi:10.1016/j.cell.2006.09.026. PMID 17081983.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • Lin D, Ippolito GC, Zong RT, Bryant J, Koslovsky J, Tucker P (2007). "Bright/ARID3A contributes to chromatin accessibility of the immunoglobulin heavy chain enhancer". Molecular Cancer. 6: 23. doi:10.1186/1476-4598-6-23. PMC 1852116. PMID 17386101.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>
  • 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. PMID 26776511. 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.<templatestyles src="Module:Citation/CS1/styles.css"></templatestyles>

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.