CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha)

2014-07-01   Tian V Tian , Thomas Graf 




Atlas Image
Figure 1: Human C/EBPa mRNA.


Human C/EBPα is an intronless gene located on the minus strand of chromosome 19q.


The C/EBPa mRNA (RNA messenger) consists of a short 5 unstranslated region (5-UTR), a unique protein coding sequence (CDS) and a long 3-UTR (Hendricks-Taylor et al., 1992).


Atlas Image
Figure 2: C/EBPa protein domains and interactions.


Human C/EBPα mRNA gives rise to two protein products by using two different translation starting sites (Figure 1 and 2) (Calkhoven et al., 2000). Compared to full-length C/EBPA protein, P42, the shorter P30 isoform lacks N-terminal 117 amino acids (Lin et al., 1993).
As a transcription factor, C/EBPA protein consists of DNA-binding domain (DBD) in its carboxyl-terminal (C-terminal), which is conserved between C/ebp family members (Leutz et al., 2011). The highly conserved C-terminus includes the basic DNA binding leucine zipper domain (bZip). The bZip domain in turn consists of a basic region that represents the DNA binding domain (DBD), the fork domain and the leucine zipper domain (LZ). The bZip domain is indispensable for homodimerization and heterodimerization with other members of the C/EBP family. This region is also involved in the interaction with other transcription factors (e.g. E2F, PU.1, c-JUN, RUNX1 and ETS1) (McNagny et al., 1998; Yamaguchi et al., 1999; Ramji and Foka, 2002; Nerlov, 2004; Koschmieder et al., 2005; Leutz et al., 2011).
The N-terminus of C/EBPa consists of three transactivation domains (TA), which can interact with components of the transcriptional machinery (e.g. CBP/P300, TBP/TFIIB) (Nerlov and Ziff, 1995; Kovacs et al., 2003; Schwartz et al., 2003), cell cycle regulators (e.g. E2F, CDK2, CDK4) (Porse et al., 2001; Porse et al., 2006) and chromatin remodellers (e.g. SWI/SNF) (Pedersen et al., 2001).


C/EBPa is mainly expressed in terminally differentiated cells, such as mature adipocytes and myelomonocytic cells. C/EBPa is also found expressed in skin, intestine, lung, adrenal gland, mammary gland, ovary, prostate, placenta (Oh and Smart, 1998; Birkenmeier et al., 1989).


C/EBPa protein is localized in nucleus.


C/EBPa homozygous null mice lack white adipose tissues (Wang et al., 1995), as well as mature granulocytes and granulocyte-macrophage precursors (Zhang et al., 1997; Heath et al., 2004). In addition, forced expression of C/EBPa can direct uncommitted progenitors to differentiate into adipocytes and granulocytes (Freytag et al., 1994; Radomska et al., 1998; Nerlov et al., 1998). Further studies suggest that C/EBPa plays important roles in lineage determination by activating lineage-specific genes (Nerlov, 2004; Graf and Enver, 2009).
In hematopoiesis, C/EBPa is one of the key factors driving myeloid cell differentiation from hematopoietic stem cells by interacting with other proteins, such as the ETS family transcription factor PU.1, the ATP dependent chromatin remodeling complex SWI/SNF, the DNA modifying enzyme TET2 (McNagny et al., 1998; Koschmieder et al., 2005; Leutz et al., 2011; Kallin et al., 2012). Ectopic expression of C/EBPa leads to cell cycle arrest via direct interaction with the key cell cycle regulators CDK2/4 and E2F (Porse et al., 2001; Porse et al., 2006). The N-terminal truncated form of C/EBPa, P30, has been shown to act as a dominant negative regulator of the full-length form, P42. Modulation of P30 expression level in mice can alter normal adipogenesis and granulopoiesis (Kirstetter et al., 2008).
Notably, ectopic expression of C/EBPa in B and T-lymphocyte precursors results in transdifferentiation into functional macrophages (Xie et al., 2004; Laiosa et al., 2006; Bussmann et al., 2009; Di Tullio et al., 2011; Kallin et al., 2012). Interestingly, C/EBPa mediated conversion of B lymphoma cells into macrophages impairs significantly its tumorigenicity, providing a novel strategy for lymphoma treatment (Rapino et al., 2013). Moreover, a recent study showed that transient C/EBPa expression is also capable of facilitating the conversion of B cells into induced pluripotent stem cells (iPS cells) (Di Stefano et al., 2014).
Moreover, C/EBPa has been shown involved in lung development and airway epithelial differentiation (Cassel et al., 2000a; Cassel et al., 2000b; Cassel et al., 2002). The conditional deletion of C/EBPa gene in respiratory epithelium results in respiratory arrest and death soon after birth. This phenotype is associated with proliferation of immature type II alveolar cells, which causes epithelial expansion and loss of air space (Martis et al., 2006; Basseres et al., 2006).


C/EBPa belongs to the CCAAT/enhancer binging protein family and is highly conserved across vertebrate species. Sequence alignments show that C/EBP members share several conserved regions including the bZip and transactivation domains (Leutz et al., 2011).



Mutations of the C/EBPα gene have been detected in 7%-15% of Acute Myeloid Leukemia (AML) (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005), around 4% of Myelodysplastic Syndrome (MDS) and Chronic Myeloid Leukemia (CML) (Shih et al., 2005). In addition, two familial cases of AML harboring C/EBPA mutations have been reported (Smith et al., 2004; Renneville et al., 2009).


Germ line mutations of C/EBPα have been described for two familial cases of AML. In one Inherited acute myeloid leukemia case, a heterozygous deletion of cytosine 212 has been reported (Smith et al., 2004). Recently, the second family contained a heterozygous insertion of cytosine at nucleotide 217 (Renneville et al., 2009). These mutations result in frameshifts, leading to a premature termination of full-length C/EBPa P42 isoform translation. Nonetheless, the alternative C/EBPa P30 isoform translation could be potentially privileged. P30 isoform has dominant-negative activity on the full-length P42 isoform.


It has been shown that 7%-15% of AML harbor somatic mutations of the C/EBPα gene (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005). In addition, C/EBPα mutations have been detected in MDS and CML patient samples. These mutations can be basically divided into two categories: C-terminal in-frame ins/del mutations altering C/EBPA DNA-binding activities, and N-terminal out-of-frame ins/del mutations impairing translation of full-length P42 isoform and leading aberrant expression of P30 isoform, which has dominant-negative activity on P42 isoform. The majority of leukemias with biallelic C/EBPA mutations harbor one allele with C-terminal mutations and the other one with N-terminal mutations. Tumors with homozygous N-terminal or C-terminal mutations are relatively rare.

Implicated in

Entity name
Mutations in C/EBPα have been identified in 7-15% of AML cases (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005). A meta-analysis of a cohort of 1175 patients reported that C/EBPα mutations are preferentially identified in M1, M2 and M4 FAB subtypes and associated with normal karyotype (Leroy et al., 2005).
It has been shown that AML patients harboring C/EBPα mutations have favorable prognosis (Preudhomme et al., 2002).
Fusion protein
C-terminal in-frame ins/del mutations can alter C/EBPa DNA-binding activities, and N-terminal out-of-frame ins/del mutations impairing translation of full-length P42 isoform and leading to aberrant expression of P30 isoform, which has dominant-negative activity on P42 isoform (Leroy et al., 2005).
Mouse models harboring biallelic (C-terminal and N-terminal) C/EBPα mutations suggested that the co-existence of these mutations can increase the proliferation of long-term hematopoietic stem cells (LT-HSC) and override normal HSC homeostasis, leading to expansion of premalignant HSC (Kirstetter et al., 2008; Bereshchenko et al., 2009). Moreover, the fusion oncoproteins AML1-ETO (t(8;21)), CBFb-HYH11 (inv(16)) and PML-RARa (t(15;17)) suppress C/EBPA mRNA expression and/or protein activity in AML (Pabst et al., 2001a; Truong et al., 2003; Cilloni et al., 2003).
Entity name
B cell precursor acute lymphoblastic leukemia (BCP-ALL)
It has been reported that C/EBPa is involved in several cases of BCP-ALL, although the prevalence of C/EBPa involved translocation need to be determined using larger cohorts (Chapiro et al., 2006; Akasaka et al., 2007; Jeffries et al., 2014). In these BCP-ALL cases, C/EBPa is aberrantly expressed by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus.
Aberrant expression of C/EBPa in BCP-ALL samples harboring t(14;19)(q32;q13) suggests that C/EBPa may have oncogenic function in this disease, which is in contrast to its onco-suppressor role in AML (Chapiro et al., 2006). Further biological studies need to be performed to clarify this hypothesis.
Entity name
Non-small-cell lung cancer
The chromosomal region including C/EBPa was reported deleted in 50% stage II and IIIA lung adenocarcinomas (Girard et al., 2000). However, mutations of C/EBPa in lung cancer are rare. It has been as well reported that an upstream promoter region of the C/EBPa gene is hypermethylated in approximately 65% of primary lung tumors (Tada et al., 2006). These evidences suggest that C/EBPa is a tumor suppressor in non-small-cell lung cancer.
Ectopic expression of C/EBPa in lung cancer cell lines results in significant growth arrest (Halmos et al., 2002; Costa et al., 2007). A transcriptional analysis identified that differentiation associated gene FoxA2 is a direct target gene of C/EBPa in lung cancer cell line (Halmos et al., 2004). Recently, using urethane-induced lung cancer model, it has been shown that C/EBPa expression is extinguished through p38alpha MAP kinase inactivation, leading to tumor progression (Sato et al., 2013), confirming a tumor suppressor role of C/EBPa in lung cancer.
Entity name
Skin squamous cell carcinoma
Although C/EBPa expression has been found in human precancerous skin lesions (Actinic Keratoses) and normal epidermis, its expression is undetectable in invasive squamous cell carcinoma samples (Thompson et al., 2011), suggesting a possible role as a tumor-suppressor in skin cancer.
In normal epidermis, C/EBPa expression is located in basal and suprabasal keratinocytes (Maytin and Habener, 1998; Thompson et al., 2011). Forced C/EBPa expression in a skin cancer cell line inhibits cell proliferation (Shim et al., 2005). Moreover, C/EBPa-null mice are highly susceptible to 7,12-dimethylbenz[a]anthracene- and UVB-induced skin tumor development (Loomis et al., 2007; Thompson et al., 2011). Notably, It has been shown that down-regulation of C/EBPa in skin cancer cells is associated with oncogenic Ras activation (Shim et al., 2005; Loomis et al., 2007).
Entity name
Prostate cancer
It has been shown that C/EBPa expression is down-regulated in prostate cancer sample comparing to normal prostate tissue (Yin et al., 2006). Interestingly, one study showed that C/EBPa expression is sequestered in cytosol, which could impair its transcription factor activity (Zhang et al., 2008). Although further studies need to be performed with larger prostate cancer cohorts for confirmation, these observations suggest an emerging tumor suppressor role of C/EBPa in prostate cancer.
C/EBPa is mainly expressed in basal layer in normal prostate. In most prostate adenocarcinoma samples, its expression level is low (Yin et al., 2006; Zhang et al., 2008). Forced expression of C/EBPa in prostate cancer cell lines can inhibit PSA (Prostate Specific Antigen) expression and regulate negatively androgen receptor (AR) signaling (Chattopadhyay et al., 2006; Yin et al., 2006; Zhang et al., 2010). In addition, in AR-negative prostate cancer cell lines, ectopically expressed C/EBPA protein can physically interact with Ku proteins (Ku70, Ku80) and Poly [ADP-ribose] polymerase 1 (PARP-1), conferring prostate cancer cells an increased sensitivity to DNA-damaging agents (Yin and Glass, 2006).
Entity name
Hepatocellular carcinoma
The expression of C/EBPa is reduced in hepatocellular carcinoma samples and higher expression of C/EBPa in hepatocellular carcinoma reversibly correlated with the tumor size and clinical stage (Tomizawa et al., 2003).
Forced C/EBPa expression in hepatoma cell lines impairs proliferation and tumorigenicity (Watkins et al., 1996). Liver specific C/EBPa knock-in mice are resistant, at least partially, to diethylnitrosamine-induced hepatocellular carcinoma formation. These observations suggest a tumor suppressor role of C/EBPa in hepatocellular carcinoma (Tan et al., 2005).
Entity name
Head and neck squamous cell cancer
It has been reported that C/EBPa expression is down-regulated in squamous cell cancers in head and neck region. This down-regulation correlates with the degree of C/EBPa promoter methylation (Bennett et al., 2007).


Pubmed IDLast YearTitleAuthors
171701242007Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).Akasaka T et al
126925182003Biallelic mutations in the CEBPA gene and low CEBPA expression levels as prognostic markers in intermediate-risk AML.Barjesteh van Waalwijk van Doorn-Khosrovani S et al
164284622006Respiratory failure due to differentiation arrest and expansion of alveolar cells following lung-specific loss of the transcription factor C/EBPalpha in mice.Bassères DS et al
175103912007Tumor suppressor activity of CCAAT/enhancer binding protein alpha is epigenetically down-regulated in head and neck squamous cell carcinoma.Bennett KL et al
198788712009Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML.Bereshchenko O et al
27927581989Tissue-specific expression, developmental regulation, and genetic mapping of the gene encoding CCAAT/enhancer binding protein.Birkenmeier EH et al
198964452009A robust and highly efficient immune cell reprogramming system.Bussmann LH et al
109219062000Translational control of C/EBPalpha and C/EBPbeta isoform expression.Calkhoven CF et al
121614232002Synergistic transactivation of the differentiation-dependent lung gene Clara cell secretory protein (secretoglobin 1a1) by the basic region leucine zipper factor CCAAT/enhancer-binding protein alpha and the homeodomain factor Nkx2.1/thyroid transcription factor-1.Cassel TN et al
107450282000C/EBPalpha and C/EBPdelta activate the clara cell secretory protein gene through interaction with two adjacent C/EBP-binding sites.Cassel TN et al
111937652000C/EBP alpha and TTF-1 synergistically transactivate the Clara cell secretory protein gene.Cassel TN et al
168736742006Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia.Chapiro E et al
164558202006The CCAAT enhancer-binding protein-alpha negatively regulates the transactivation of androgen receptor in prostate cancer cells.Chattopadhyay S et al
145040762003Down-modulation of the C/EBPalpha transcription factor in core binding factor acute myeloid leukemias.Cilloni D et al
172399842007Immunohistochemical analysis of C/EBPalpha in non-small cell lung cancer reveals frequent down-regulation in stage II and IIIA tumors: a correlative study of E3590.Costa DB et al
243362022014C/EBPα poises B cells for rapid reprogramming into induced pluripotent stem cells.Di Stefano B et al
219695812011CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.Di Tullio A et al
79588461994Ectopic expression of the CCAAT/enhancer-binding protein alpha promotes the adipogenic program in a variety of mouse fibroblastic cells.Freytag SO et al
147265042004CEBPA mutations in younger adults with acute myeloid leukemia and normal cytogenetics: prognostic relevance and analysis of cooperating mutations.Fröhling S et al
109873042000Genome-wide allelotyping of lung cancer identifies new regions of allelic loss, differences between small cell lung cancer and non-small cell lung cancer, and loci clustering.Girard L et al
199562532009Forcing cells to change lineages.Graf T et al
152053242004A transcriptional profiling study of CCAAT/enhancer binding protein targets identifies hepatocyte nuclear factor 3 beta as a novel tumor suppressor in lung cancer.Halmos B et al
118097052002Down-regulation and antiproliferative role of C/EBPalpha in lung cancer.Halmos B et al
150730372004C/EBPalpha deficiency results in hyperproliferation of hematopoietic progenitor cells and disrupts macrophage development in vitro and in vivo.Heath V et al
14278191992The CCAAT/enhancer binding protein (C/EBP alpha) gene (CEBPA) maps to human chromosome 19q13.1 and the related nuclear factor NF-IL6 (C/EBP beta) gene (CEBPB) maps to human chromosome 20q13.1.Hendricks-Taylor LR et al
248162342014IGH@ translocations co-exist with other primary rearrangements in B-cell precursor acute lymphoblastic leukemia.Jeffries SJ et al
229818652012Tet2 facilitates the derepression of myeloid target genes during CEBPα-induced transdifferentiation of pre-B cells.Kallin EM et al
183945532008Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells.Kirstetter P et al
161588162005Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia.Koschmieder S et al
128577542003CCAAT/enhancer-binding protein family members recruit the coactivator CREB-binding protein and trigger its phosphorylation.Kovács KA et al
170880842006Reprogramming of committed T cell progenitors to macrophages and dendritic cells by C/EBP alpha and PU.1 transcription factors.Laiosa CV et al
156743662005CEBPA point mutations in hematological malignancies.Leroy H et al
213269022011Crosstalk between phosphorylation and multi-site arginine/lysine methylation in C/EBPs.Leutz A et al
84157481993A 30-kDa alternative translation product of the CCAAT/enhancer binding protein alpha message: transcriptional activator lacking antimitotic activity.Lin FT et al
157460352005Characterization of CEBPA mutations in acute myeloid leukemia: most patients with CEBPA mutations have biallelic mutations and show a distinct immunophenotype of the leukemic cells.Lin LI et al
176388882007Genetic ablation of CCAAT/enhancer binding protein alpha in epidermis reveals its role in suppression of epithelial tumorigenesis.Loomis KD et al
164673602006C/EBPalpha is required for lung maturation at birth.Martis PC et al
95064421998Transcription factors C/EBP alpha, C/EBP beta, and CHOP (Gadd153) expressed during the differentiation program of keratinocytes in vitro and in vivo.Maytin EV et al
96494371998Regulation of eosinophil-specific gene expression by a C/EBP-Ets complex and GATA-1.McNagny KM et al
96948051998Distinct C/EBP functions are required for eosinophil lineage commitment and maturation.Nerlov C et al
75560731995CCAAT/enhancer binding protein-alpha amino acid motifs with dual TBP and TFIIB binding ability co-operate to activate transcription in both yeast and mammalian cells.Nerlov C et al
151222102004C/EBPalpha mutations in acute myeloid leukaemias.Nerlov C et al
96203021998Expression of CCAAT/enhancer binding proteins (C/EBP) is associated with squamous differentiation in epidermis and isolated primary keratinocytes and is altered in skin neoplasms.Oh HS et al
112421072001Dominant-negative mutations of CEBPA, encoding CCAAT/enhancer binding protein-alpha (C/EBPalpha), in acute myeloid leukemia.Pabst T et al
117314832001Cooperation between C/EBPalpha TBP/TFIIB and SWI/SNF recruiting domains is required for adipocyte differentiation.Pedersen TA et al
164284552006The proline-histidine-rich CDK2/CDK4 interaction region of C/EBPalpha is dispensable for C/EBPalpha-mediated growth regulation in vivo.Porse BT et al
123513772002Favorable prognostic significance of CEBPA mutations in patients with de novo acute myeloid leukemia: a study from the Acute Leukemia French Association (ALFA).Preudhomme C et al
96328141998CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors.Radomska HS et al
120061032002CCAAT/enhancer-binding proteins: structure, function and regulation.Ramji DP et al
235454982013C/EBPα induces highly efficient macrophage transdifferentiation of B lymphoma and leukemia cell lines and impairs their tumorigenicity.Rapino F et al
189464942009Another pedigree with familial acute myeloid leukemia and germline CEBPA mutation.Renneville A et al
234372972013CCAAT/enhancer-binding protein-α suppresses lung tumor development in mice through the p38α MAP kinase pathway.Sato A et al
125741242003Recruitment of p300 by C/EBPbeta triggers phosphorylation of p300 and modulates coactivator activity.Schwartz C et al
157560052005Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia.Shih LY et al
157058842005Diminished expression of C/EBPalpha in skin carcinomas is linked to oncogenic Ras and reexpression of C/EBPalpha in carcinoma cells inhibits proliferation.Shim M et al
155750562004Mutation of CEBPA in familial acute myeloid leukemia.Smith ML et al
126610072003Mutations of CEBPA in acute myeloid leukemia FAB types M1 and M2.Snaddon J et al
165378322006Epigenetic modulation of tumor suppressor CCAAT/enhancer binding protein alpha activity in lung cancer.Tada Y et al
162880222005CCAAT/enhancer binding protein alpha knock-in mice exhibit early liver glycogen storage and reduced susceptibility to hepatocellular carcinoma.Tan EH et al
213467722011C/EBPα expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBPα confers susceptibility to UVB-induced skin squamous cell carcinomas.Thompson EA et al
126802362003Down-regulated expression of the CCAAT/enhancer binding protein alpha and beta genes in human hepatocellular carcinoma: a possible prognostic marker.Tomizawa M et al
123934502003CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia.Truong BT et al
76525571995Impaired energy homeostasis in C/EBP alpha knockout mice.Wang ND et al
86407621996Impaired proliferation and tumorigenicity induced by CCAAT/enhancer-binding protein.Watkins PJ et al
151634132004Stepwise reprogramming of B cells into macrophages.Xie H et al
104387311999C/EBPbeta and GATA-1 synergistically regulate activity of the eosinophil granule major basic protein promoter: implication for C/EBPbeta activity in eosinophil gene expression.Yamaguchi Y et al
164907872006In prostate cancer cells the interaction of C/EBPalpha with Ku70, Ku80, and poly(ADP-ribose) polymerase-1 increases sensitivity to DNA damage.Yin H et al
167746852006Down regulation of PSA by C/EBPalpha is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell line.Yin H et al
90128251997Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice.Zhang DE et al
199019622010C/EBPalpha redirects androgen receptor signaling through a unique bimodal interaction.Zhang J et al
184812682008Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the prostate.Zhang J et al

Other Information

Locus ID:

NCBI: 1050
MIM: 116897
HGNC: 1833
Ensembl: ENSG00000245848


dbSNP: 1050
ClinVar: 1050
TCGA: ENSG00000245848


Gene IDTranscript IDUniprot

Expression (GTEx)



PathwaySourceExternal ID
Acute myeloid leukemiaKEGGko05221
Pathways in cancerKEGGhsa05200
Acute myeloid leukemiaKEGGhsa05221
Transcriptional misregulation in cancerKEGGko05202
Transcriptional misregulation in cancerKEGGhsa05202
Non-alcoholic fatty liver disease (NAFLD)KEGGhsa04932
Non-alcoholic fatty liver disease (NAFLD)KEGGko04932
Developmental BiologyREACTOMER-HSA-1266738
Transcriptional regulation of white adipocyte differentiationREACTOMER-HSA-381340

Protein levels (Protein atlas)

Not detected


Pubmed IDYearTitleCitations
184506022008Mutations and treatment outcome in cytogenetically normal acute myeloid leukemia.422
163255772005A minicircuitry comprised of microRNA-223 and transcription factors NFI-A and C/EBPalpha regulates human granulopoiesis.358
109219062000Translational control of C/EBPalpha and C/EBPbeta isoform expression.191
241079922013DNMT1-interacting RNAs block gene-specific DNA methylation.188
160768672005Nucleophosmin gene mutations are predictors of favorable prognosis in acute myelogenous leukemia with a normal karyotype.143
191718802009Double CEBPA mutations, but not single CEBPA mutations, define a subgroup of acute myeloid leukemia with a distinctive gene expression profile that is uniquely associated with a favorable outcome.136
188096072008Prognostic significance of, and gene and microRNA expression signatures associated with, CEBPA mutations in cytogenetically normal acute myeloid leukemia with high-risk molecular features: a Cancer and Leukemia Group B Study.125
84157481993A 30-kDa alternative translation product of the CCAAT/enhancer binding protein alpha message: transcriptional activator lacking antimitotic activity.100
206251122010Ablation of C/EBP homologous protein attenuates endoplasmic reticulum-mediated apoptosis and cardiac dysfunction induced by pressure overload.93
123513772002Favorable prognostic significance of CEBPA mutations in patients with de novo acute myeloid leukemia: a study from the Acute Leukemia French Association (ALFA).90


Tian V Tian ; Thomas Graf

CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha)

Atlas Genet Cytogenet Oncol Haematol. 2014-07-01

Online version:

Historical Card

2006-05-01 CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha) by  Lan-Lan Smith 

Cancer Research UK Medical Oncology Unit, Charterhouse Square, Barts, the London School of Medicine, Dentistry, London, UK