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Open Access Articles- Top Results for ARID3A

ARID3A

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Identifiers
SymbolsARID3A ; BRIGHT; DRIL1; DRIL3; E2FBP1
External IDsOMIM603265 MGI1328360 HomoloGene124247 GeneCards: ARID3A Gene
RNA expression pattern
File:PBB GE ARID3A 205865 at tn.png
More reference expression data
Orthologs
SpeciesHumanMouse
Entrez182013496
EnsemblENSG00000116017ENSMUSG00000019564
UniProtQ99856Q62431
RefSeq (mRNA)NM_005224NM_001288625
RefSeq (protein)NP_005215NP_001275554
Location (UCSC)Chr 19:
0.93 – 0.98 Mb
Chr 10:
79.93 – 79.96 Mb
PubMed search[1][2]

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 (Nov 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. PMID 9722953. doi:10.1006/geno.1998.5259. 
  2. ^ a b "Entrez Gene: ARID3A AT rich interactive domain 3A (BRIGHT-like)". 
  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". Cell. Immunol. 228 (1): 42–53. PMID 15203319. doi:10.1016/j.cellimm.2004.03.004. 
  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. PMID 9780002. doi:10.1038/sj.onc.1202163. 

Further reading

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External links

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

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