AEBP2

AE binding protein 2
Identifiers
Symbol AEBP2
External IDs HomoloGene: 40690 GeneCards: AEBP2 Gene
Orthologs
Species Human Mouse
Entrez 121536 11569
Ensembl ENSG00000139154 ENSMUSG00000030232
UniProt Q6ZN18 Q9Z248
RefSeq (mRNA) NM_001114176 NM_001005605
RefSeq (protein) NP_001107648 NP_001005605
Location (UCSC) Chr 12:
19.4 – 19.72 Mb
Chr 6:
140.62 – 140.68 Mb
PubMed search

Adipocyte Enhancer-Binding Protein is a zinc finger protein that in humans is encoded by the evolutionarily well-conserved gene AEBP2. It was initially identified due to its binding capability to the promoter[1] of the adipocyte P2 gene, and was therefore named Adipocyte Enhancer Binding Protein 2. AEBP2 is a potential targeting protein for the mammalian Polycomb Repression Complex 2 (PRC2).[2]

Function

AEBP2 is a DNA-binding transcriptional repressor. It may interact with and stimulate the activity of the PRC2 complex.[3]

AEBP2 may regulate the migration and development of the neural crest cells through the PRC2-mediated epigenetic mechanism and is most likely a targeting protein for the mammalian PRC2 complex.[4]

Clinical significance

Diseases associated with AEBP2 include Waardenburg's syndrome, and Hirschsprung's disease.[4]

References

  1. Imhof, Axel; Kim, Hana; Bakshi, Arundhati; Kim, Joomyeong (2015). "Retrotransposon-Derived Promoter of Mammalian Aebp2". PLOS ONE 10 (4): e0126966. doi:10.1371/journal.pone.0126966. ISSN 1932-6203.
  2. Kim H, Kang K, Ekram MB, Roh TY, Kim J (2011). "Aebp2 as an epigenetic regulator for neural crest cells". PLoS ONE 6 (9): e25174. doi:10.1371/journal.pone.0025174. PMID 21949878.
  3. Cao R, Zhang Y (July 2004). "SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex". Mol. Cell 15 (1): 57–67. doi:10.1016/j.molcel.2004.06.020. PMID 15225548.
  4. 1 2 Kim H, Kang K, Kim J (2009). "AEBP2 as a potential targeting protein for Polycomb Repression Complex PRC2". Nucleic Acids Res. 37 (9): 2940–50. doi:10.1093/nar/gkp149. PMID 19293275.


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