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CCAAT/enhancer binding protein (C/EBP), epsilon
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols CEBPE ; C/EBP-epsilon; CRP1
External IDs OMIM600749 MGI103572 HomoloGene1367 GeneCards: CEBPE Gene
RNA expression pattern
PBB GE CEBPE 214523 at tn.png
More reference expression data
Species Human Mouse
Entrez 1053 110794
Ensembl ENSG00000092067 ENSMUSG00000052435
UniProt Q15744 Q6PZD9
RefSeq (mRNA) NM_001805 NM_207131
RefSeq (protein) NP_001796 NP_997014
Location (UCSC) Chr 14:
23.12 – 23.12 Mb
Chr 14:
54.71 – 54.71 Mb
PubMed search [1] [2]

CCAAT/enhancer binding protein (C/EBP), epsilon, also known as CEBPE and CRP1, is a type of ccaat-enhancer-binding protein. CEBPE is its human gene[1][2] and is pro-apoptotic.[3]

The protein encoded by this gene is a bZIP transcription factor which can bind as a homodimer to certain DNA regulatory regions. It can also form heterodimers with the related protein CEBP-δ. The encoded protein may be essential for terminal differentiation and functional maturation of committed granulocyte progenitor cells. Mutations in this gene have been associated with specific granule deficiency, a rare congenital disorder. Multiple variants of this gene have been described, but the full-length nature of only one has been determined.[1]


  1. ^ a b "Entrez Gene: CEBPE CCAAT/enhancer binding protein (C/EBP), epsilon". 
  2. ^ Antonson P, Stellan B, Yamanaka R, Xanthopoulos KG (Jul 1996). "A novel human CCAAT/enhancer binding protein gene, C/EBPepsilon, is expressed in cells of lymphoid and myeloid lineages and is localized on chromosome 14q11.2 close to the T-cell receptor alpha/delta locus". Genomics 35 (1): 30–8. doi:10.1006/geno.1996.0319. PMID 8661101. 
  3. ^ Nakajima H, Watanabe N, Shibata F, Kitamura T, Ikeda Y, Handa M (May 2006). "N-terminal region of CCAAT/enhancer-binding protein epsilon is critical for cell cycle arrest, apoptosis, and functional maturation during myeloid differentiation". The Journal of Biological Chemistry 281 (20): 14494–502. doi:10.1074/jbc.M600575200. PMID 16531405. 

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