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AT rich interactive domain 4A (RBP1-like)
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols ARID4A ; RBBP-1; RBBP1; RBP-1; RBP1
External IDs OMIM180201 MGI2444354 HomoloGene11303 GeneCards: ARID4A Gene
RNA expression pattern
PBB GE ARID4A 205062 x at tn.png
More reference expression data
Species Human Mouse
Entrez 5926 238247
Ensembl ENSG00000032219 ENSMUSG00000048118
UniProt P29374 E9Q9V1
RefSeq (mRNA) NM_002892 NM_001081195
RefSeq (protein) NP_002883 NP_001074664
Location (UCSC) Chr 14:
58.3 – 58.37 Mb
Chr 12:
71.02 – 71.1 Mb
PubMed search [1] [2]

AT rich interactive domain 4A (RBP1-like), also known as ARID4A, is a protein which in humans is encoded by the ARID4A gene.[1][2][3]


The protein encoded by this gene is a ubiquitously expressed nuclear protein. It binds directly, with several other proteins, to retinoblastoma protein (pRB) which regulates cell proliferation. pRB represses transcription by recruiting the encoded protein. This protein, in turn, serves as a bridging molecule to recruit HDACs and, in addition, provides a second HDAC-independent repression function. The encoded protein possesses transcriptional repression activity. Multiple alternatively spliced transcripts have been observed for this gene, although not all transcript variants have been fully described.[1]

Model organisms[edit]

Model organisms have been used in the study of ARID4A function. A conditional knockout mouse line, called Arid4atm1a(EUCOMM)Wtsi[14][15] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists — at the Wellcome Trust Sanger Institute.[16][17][18] Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[12][19]

Twenty five tests were carried out and nine phenotypes were reported. Fewer homozygous mutant embryos were identified during gestation than expected, and in a separate study less than the predicted Mendelian ratio survived until weaning. Homozygous mutant male adults has a reduced body weight curve and a decreased grip strength. Homozygous mutant adults of both sexes had a decreased body weight as determined by DEXA, displayed vertebral fusion and had clinical chemistry abnormalities including hypoalbuminemia and decreased circulating fructosamine levels. They also had haematological defects and an increased NK cell number.[12]


ARID4A has been shown to interact with Retinoblastoma protein.[20]


  1. ^ a b "Entrez Gene: ARID4A AT rich interactive domain 4A (RBP1-like)". 
  2. ^ Defeo-Jones D, Huang PS, Jones RE, Haskell KM, Vuocolo GA, Hanobik MG, Huber HE, Oliff A (Jul 1991). "Cloning of cDNAs for cellular proteins that bind to the retinoblastoma gene product". Nature 352 (6332): 251–4. doi:10.1038/352251a0. PMID 1857421. 
  3. ^ Otterson GA, Kratzke RA, Lin AY, Johnston PG, Kaye FJ (Apr 1993). "Alternative splicing of the RBP1 gene clusters in an internal exon that encodes potential phosphorylation sites". Oncogene 8 (4): 949–57. PMID 8455946. 
  4. ^ "Body weight data for Arid4a". Wellcome Trust Sanger Institute. 
  5. ^ "Grip strength data for Arid4a". Wellcome Trust Sanger Institute. 
  6. ^ "DEXA data for Arid4a". Wellcome Trust Sanger Institute. 
  7. ^ "Radiography data for Arid4a". Wellcome Trust Sanger Institute. 
  8. ^ "Clinical chemistry data for Arid4a". Wellcome Trust Sanger Institute. 
  9. ^ "Haematology data for Arid4a". Wellcome Trust Sanger Institute. 
  10. ^ "Salmonella infection data for Arid4a". Wellcome Trust Sanger Institute. 
  11. ^ "Citrobacter infection data for Arid4a". Wellcome Trust Sanger Institute. 
  12. ^ a b c Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x. 
  13. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  14. ^ "International Knockout Mouse Consortium". 
  15. ^ "Mouse Genome Informatics". 
  16. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750. 
  17. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718. 
  18. ^ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. 
  19. ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353. 
  20. ^ Lai A, Lee JM, Yang WM, DeCaprio JA, Kaelin WG, Seto E, Branton PE (Oct 1999). "RBP1 recruits both histone deacetylase-dependent and -independent repression activities to retinoblastoma family proteins". Molecular and Cellular Biology 19 (10): 6632–41. doi:10.1128/mcb.19.10.6632. PMC 84642. PMID 10490602. 

Further reading[edit]

External links[edit]

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