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]
References
- ^ a b "Entrez Gene: CEBPE CCAAT/enhancer binding protein (C/EBP), epsilon".
- ^ Antonson P, Stellan B, Yamanaka R, Xanthopoulos KG (July 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.
- ^ 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". J. Biol. Chem. 281 (20): 14494–502. doi:10.1074/jbc.M600575200. PMID 16531405.
Further reading
- Sladek FM, Darnell JE (1992). "Mechanisms of liver-specific gene expression.". Curr. Opin. Genet. Dev. 2 (2): 256–9. doi:10.1016/S0959-437X(05)80282-5. PMID 1638120.
- Gombart AF, Koeffler HP (2002). "Neutrophil specific granule deficiency and mutations in the gene encoding transcription factor C/EBP(epsilon).". Curr. Opin. Hematol. 9 (1): 36–42. doi:10.1097/00062752-200201000-00007. PMID 11753076.
- Williams SC, Cantwell CA, Johnson PF (1991). "A family of C/EBP-related proteins capable of forming covalently linked leucine zipper dimers in vitro.". Genes Dev. 5 (9): 1553–67. doi:10.1101/gad.5.9.1553. PMID 1884998.
- Antonson P, Stellan B, Yamanaka R, Xanthopoulos KG (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.
- Chumakov AM, Grillier I, Chumakova E et al. (1997). "Cloning of the novel human myeloid-cell-specific C/EBP-epsilon transcription factor.". Mol. Cell. Biol. 17 (3): 1375–86. PMC 231862. PMID 9032264.
- Yamanaka R, Kim GD, Radomska HS et al. (1997). "CCAAT/enhancer binding protein epsilon is preferentially up-regulated during granulocytic differentiation and its functional versatility is determined by alternative use of promoters and differential splicing.". Proc. Natl. Acad. Sci. U.S.A. 94 (12): 6462–7. doi:10.1073/pnas.94.12.6462. PMC 21072. PMID 9177240.
- Verbeek W, Gombart AF, Chumakov AM et al. (1999). "C/EBPepsilon directly interacts with the DNA binding domain of c-myb and cooperatively activates transcription of myeloid promoters.". Blood 93 (10): 3327–37. PMID 10233885.
- Lekstrom-Himes JA, Dorman SE, Kopar P et al. (1999). "Neutrophil-specific granule deficiency results from a novel mutation with loss of function of the transcription factor CCAAT/enhancer binding protein epsilon.". J. Exp. Med. 189 (11): 1847–52. doi:10.1084/jem.189.11.1847. PMC 2193089. PMID 10359588.
- Tavor S, Vuong PT, Park DJ et al. (2002). "Macrophage functional maturation and cytokine production are impaired in C/EBP epsilon-deficient mice.". Blood 99 (5): 1794–801. doi:10.1182/blood.V99.5.1794. PMID 11861297.
- Zhang P, Nelson E, Radomska HS et al. (2002). "Induction of granulocytic differentiation by 2 pathways.". Blood 99 (12): 4406–12. doi:10.1182/blood.V99.12.4406. PMID 12036869.
- Kim J, Cantwell CA, Johnson PF et al. (2002). "Transcriptional activity of CCAAT/enhancer-binding proteins is controlled by a conserved inhibitory domain that is a target for sumoylation.". J. Biol. Chem. 277 (41): 38037–44. doi:10.1074/jbc.M207235200. PMID 12161447.
- Du J, Stankiewicz MJ, Liu Y et al. (2003). "Novel combinatorial interactions of GATA-1, PU.1, and C/EBPepsilon isoforms regulate transcription of the gene encoding eosinophil granule major basic protein.". J. Biol. Chem. 277 (45): 43481–94. doi:10.1074/jbc.M204777200. PMID 12202480.
- Truong BT, Lee YJ, Lodie TA et al. (2003). "CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia.". Blood 101 (3): 1141–8. doi:10.1182/blood-2002-05-1374. PMID 12393450.
- Strausberg RL, Feingold EA, Grouse LH et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899–903. doi:10.1073/pnas.242603899. PMC 139241. PMID 12477932.
- Gombart AF, Kwok SH, Anderson KL et al. (2003). "Regulation of neutrophil and eosinophil secondary granule gene expression by transcription factors C/EBP epsilon and PU.1.". Blood 101 (8): 3265–73. doi:10.1182/blood-2002-04-1039. PMID 12515729.
- Khanna-Gupta A, Zibello T, Sun H et al. (2003). "Chromatin immunoprecipitation (ChIP) studies indicate a role for CCAAT enhancer binding proteins alpha and epsilon (C/EBP alpha and C/EBP epsilon ) and CDP/cut in myeloid maturation-induced lactoferrin gene expression.". Blood 101 (9): 3460–8. doi:10.1182/blood-2002-09-2767. PMID 12522000.
- Gery S, Gombart AF, Fung YK, Koeffler HP (2004). "C/EBPepsilon interacts with retinoblastoma and E2F1 during granulopoiesis.". Blood 103 (3): 828–35. doi:10.1182/blood-2003-01-0159. PMID 12947005.
- Gery S, Park DJ, Vuong PT et al. (2005). "Retinoic acid regulates C/EBP homologous protein expression (CHOP), which negatively regulates myeloid target genes.". Blood 104 (13): 3911–7. doi:10.1182/blood-2003-10-3688. PMID 15308577.
External links
- CEBPE protein, human at the US National Library of Medicine Medical Subject Headings (MeSH)
This article incorporates text from the United States National Library of Medicine, which is in the public domain.
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