Product: C/EBP alpha Antibody
Catalog: AF6333
Description: Rabbit polyclonal antibody to C/EBP alpha
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine
Mol.Wt.: 30,43kDa; 38kD(Calculated).
Uniprot: P49715
RRID: AB_2835189

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Pig(100%), Bovine(100%)
C/EBP alpha Antibody detects endogenous levels of total C/EBP alpha.
Cite Format: Affinity Biosciences Cat# AF6333, RRID:AB_2835189.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Apoptotic cysteine protease; Apoptotic protease Mch 5; C/EBP alpha; C/ebpalpha; CAP4; Caspase 8 precursor; CBF-A; CCAAT Enhancer Binding Protein alpha; CCAAT/enhancer binding protein (C/EBP), alpha; CCAAT/enhancer-binding protein alpha; CEBP; CEBP A; CEBP alpha; Cebpa; CEBPA_HUMAN; FADD homologous ICE/CED 3 like protease; FADD like ICE; FLICE; ICE like apoptotic protease 5; ICE8; MACH; MCH5; MORT1 associated CED 3 homolog;


The protein encoded by this intronless gene is a bZIP transcription factor which can bind as a homodimer to certain promoters and enhancers. It can also form heterodimers with the related proteins CEBP-beta and CEBP-gamma. The encoded protein has been shown to bind to the promoter and modulate the expression of the gene encoding leptin, a protein that plays an important role in body weight homeostasis.



Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P49715 As Substrate

Site PTM Type Enzyme
S21 Phosphorylation P28482 (MAPK1) , P27361 (MAPK3) , P06493 (CDK1)
K161 Acetylation
K161 Sumoylation
K161 Ubiquitination
S190 Phosphorylation
T226 Phosphorylation
S234 Phosphorylation P06493 (CDK1)
S266 Phosphorylation
S277 Phosphorylation
K298 Acetylation
S299 Phosphorylation
K302 Acetylation
K313 Ubiquitination
K326 Acetylation
S332 Phosphorylation

Research Backgrounds


Transcription factor that coordinates proliferation arrest and the differentiation of myeloid progenitors, adipocytes, hepatocytes, and cells of the lung and the placenta. Binds directly to the consensus DNA sequence 5'-T[TG]NNGNAA[TG]-3' acting as an activator on distinct target genes. During early embryogenesis, plays essential and redundant functions with CEBPB. Essential for the transition from common myeloid progenitors (CMP) to granulocyte/monocyte progenitors (GMP). Critical for the proper development of the liver and the lung (By similarity). Necessary for terminal adipocyte differentiation, is required for postnatal maintenance of systemic energy homeostasis and lipid storage (By similarity). To regulate these different processes at the proper moment and tissue, interplays with other transcription factors and modulators. Downregulates the expression of genes that maintain cells in an undifferentiated and proliferative state through E2F1 repression, which is critical for its ability to induce adipocyte and granulocyte terminal differentiation. Reciprocally E2F1 blocks adipocyte differentiation by binding to specific promoters and repressing CEBPA binding to its target gene promoters. Proliferation arrest also depends on a functional binding to SWI/SNF complex. In liver, regulates gluconeogenesis and lipogenesis through different mechanisms. To regulate gluconeogenesis, functionally cooperates with FOXO1 binding to IRE-controlled promoters and regulating the expression of target genes such as PCK1 or G6PC. To modulate lipogenesis, interacts and transcriptionally synergizes with SREBF1 in promoter activation of specific lipogenic target genes such as ACAS2. In adipose tissue, seems to act as FOXO1 coactivator accessing to ADIPOQ promoter through FOXO1 binding sites (By similarity).

Can act as dominant-negative. Binds DNA and have transctivation activity, even if much less efficiently than isoform 2. Does not inhibit cell proliferation.

Directly and specifically enhances ribosomal DNA transcription interacting with RNA polymerase I-specific cofactors and inducing histone acetylation.


Phosphorylation at Ser-190 is required for interaction with CDK2, CDK4 and SWI/SNF complex leading to cell cycle inhibition. Dephosphorylated at Ser-190 by protein phosphatase 2A (PP2A) through PI3K/AKT signaling pathway regulation. Phosphorylation at Thr-226 and Thr-230 by GSK3 is constitutive in adipose tissue and lung. In liver, both Thr-226 and Thr-230 are phosphorylated only during feeding but not during fasting. Phosphorylation of the GSK3 consensus sites selectively decreases transactivation activity on IRE-controlled promoters.

Sumoylated, sumoylation blocks the inhibitory effect on cell proliferation by disrupting the interaction with SMARCA2.

Ubiquitinated by COP1 upon interaction with TRIB1.

Subcellular Location:



Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Binds DNA as a homodimer and as a heterodimer. Can form stable heterodimers with CEBPB, CEBPD, CEBPE and CEBPG (By similarity). Interacts with PRDM16 (By similarity). Interacts with UBN1. Interacts with ZNF638; this interaction increases transcriptional activation (By similarity). Interacts with the complex TFDP2:E2F1; the interaction prevents CEBPA binding to target gene promoters and represses its transcriptional activity. Interacts with RB1. Interacts (when phosphorylated at SER-190) with CDK2, CDK4, E2F4 and SMARCA2. Interacts with SREBPF1 (By similarity). Interacts with FOXO1 (via the Fork-head domain); the interaction increases when FOXO1 is deacetylated (By similarity). Isoform 1 and isoform 4 interacts with TAF1A and UBTF. Isoform 4 interacts with NPM1. Interacts (via recognition sequence) with TRIB1.

(Microbial infection) Interacts with HBV protein X.


The recognition sequence (54-72) is required for interaction with TRIB1.

Belongs to the bZIP family. C/EBP subfamily.

Research Fields

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)


1). Adipose specific aptamer adipo-8 recognizes and interacts with APMAP to ameliorates fat deposition in vitro and in vivo. LIFE SCIENCES, 2020 (PubMed: 32272180) [IF=6.1]

Application: WB    Species: mouse    Sample: adipocytes

Fig. 5.| Adipo-8 ameliorated fat deposition through interaction with APMAP: (C) Expression of fat metabolism related proteins: aP2, PPAR-γ, and C/EBP-α down-regulated by adipo-8 in APMAP-NC adipocytes, but not in APMAP-silent adipocytes. Control, library and adipo-8(0.01 μg/g/day for 21 days) in high fat fed mice: adipo-8 reduced body weight of HFD fed mice (P < 0.05) (D), decrease adipocytes volume (E), lowered TG(*P < 0.05) (F), but not TC (**P > 0.05) (G)without liver or renal function damage (**P > 0.05) (H).

2). Bmp8a deletion leads to obesity through regulation of lipid metabolism and adipocyte differentiation. Communications Biology, 2023 (PubMed: 37553521) [IF=5.9]

Application: WB    Species: Mouse    Sample: 3T3-L1 cells

Fig. 3 Stably overexpressing zebrafish bmp8a or mouse Bmp8a inhibits adipogenesis. a Protocol for effective differentiation of 3T3-L1 cells into adipocytes. b The mRNA expression pattern of mouse Bmp8a, Pparγ and C/ebpα during 3T3-L1 cells differentiated into adipocytes (n = 3). c, d Immunoblot analysis of mouse BMP8A protein expression in 3T3-L1 cells (Mock), stably overexpressed empty plasmid in 3T3-L1 cells (LV-ZsGreen1), stably overexpressed mouse Bmp8a in 3T3-L1 cells (LV-Bmp8a), 3T3-L1 cells infected with scramble shRNA lentivirus (LV-shRNA-scrambled), and knockdown mouse Bmp8a in 3T3-L1 cells (shRNA-Bmp8a#1 and shRNA-Bmp8a#2). BMP8A protein expression levels were quantified by ImageJ software and normalized to the amount of β-actin (d, n = 3). e, f After induction of adipogenic differentiation, differentiated 3T3-L1 adipocytes (Mock, LV-ZsGreen1, LV-bmp8a, and LV-Bmp8a) were stained with Oil Red O and subjected to OD492 quantifications (n = 3). Scale bar = 20 µm. g–j On the day after induction as indicated, expressions of adipogenic genes (Cebpα, Pparγ, and Fasn) were examined at the mRNA level by qPCR (n = 3). k–m On the day after induction, as indicated, the protein levels of PPARγ and C/EBPα detected by Immunoblot. Protein expression levels were quantified using ImageJ software and normalized to the amount of β-actin (l, m, n = 3). Data were representative of at least three independent experiments. Data were analyzed by One-way ANOVA and presented as mean ± SD

3). BMP8B Activates Both SMAD2/3 and NF-κB Signals to Inhibit the Differentiation of 3T3-L1 Preadipocytes into Mature Adipocytes. Nutrients, 2023 (PubMed: 38201894) [IF=5.9]

4). Polysaccharides from Cyclocarya paliurus: Chemical composition and lipid-lowering effect on rats challenged with high-fat diet. Journal of Functional Foods, 2017 [IF=5.6]

5). miR‑139‑5p affects cell proliferation, migration and adipogenesis by targeting insulin‑like growth factor 1 receptor in hemangioma stem cells. INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 2020 (PubMed: 31894289) [IF=5.4]

Application: WB    Species: human    Sample: HemSCs

Figure 5. |miR‑139‑5p modulated HemSCs differentiation into adipocytes through IGF‑1/IGF‑1R. (A) Adipogenic differentiation of HemSCs was determined by oil red o staining to visualize intracellular lipid droplet accumulation. (B) Oil red o‑stained cells were quantified using ImageJ software. (C) Western blot analysis demonstrated the expression levels of (D) PPAR‑γ, (E) C/EBPα and (F) C/EBPβ in HemSCs transfected with miR‑139‑5p mimics or inhibitor and treated with or without 100 ng/ml IGF‑1.

6). C/EBPα-Mediated Transcriptional Activation of PIK3C2A Regulates Autophagy, Matrix Metalloproteinase Expression, and Phenotypic of Vascular Smooth Muscle Cells in Aortic Dissection. Journal of Immunology Research, 2022 (PubMed: 36132983) [IF=4.1]

Application: WB    Species: Rat    Sample: aorta tissues

Figure 1 Establishment of aortic dissection rats reveals model-specific patterns of C/EBPα, PIK3C2A, LC3, and MMPs proteins. (a) The pathological changes in aorta tissues evaluated by H&E staining (scale bar = 500 μm). (b) Representative images of C/EBPα, PIK3C2A, LC3, MMP-2, and MMP-9 protein expression in aortic dissection rings determined by Western blot. (c) The expression level of indicated proteins

7). Equisetin inhibits adiposity through AMPK-dependent regulation of brown adipocyte differentiation. Heliyon, 2024 (PubMed: 38327434) [IF=4.0]

8). C/EBPα-mediated transcriptional activation of miR-134-5p entails KPNA3 inhibition and modulates focal hypoxic-ischemic brain damage in neonatal rats. BRAIN RESEARCH BULLETIN, 2020 (PubMed: 32814091) [IF=3.8]

9). Autologous decellularized extracellular matrix promotes adipogenic differentiation of adipose derived stem cells in low serum culture system by regulating the ERK1/2-PPARγ pathway. Adipocyte, 2021 (PubMed: 33825675) [IF=3.3]

Application: WB    Species: Human    Sample: ADSCs

Figure 5. Relation between ERK1/2 and adipogenic genes in the undifferentiated ADSCs. A. ADSCs at the 5th passage were cultured in 2% FBS on the plastic or d-ECM substrates, and the mRNA levels of PPARγ (a) and C/EPBα (b) were examined on days 1–3, respectively. Cells in 10% FBS were used as control group. N = 3. *, p < 0.05, vs. 10% FBS group; **, p < 0.01, vs. 10% FBS group; ##, p < 0.01, vs. 2% FBS group; &&, p < 0.01, vs. 10% FBS group on day 1. B. ADSCs were treated with 2% FBS and/or d-ECM. Cells without any treatment were set as control. For d-ECM treatment group, a copy pretreated with 50 μM PD98059 was established to inhibit ERK1/2 signalling (a). Afterwards, the phosphorylation of ERK1/2 (b), and the expression levels of PPARγ (c) and C/EPBα (d) were examined by Western blotting analysis. Equal loading of proteins was demonstrated by GAPDH. N = 3. *, p < 0.05, vs. 10% FBS group; **, p < 0.01, vs. 10% FBS group; ##, p < 0.01, vs. 2% FBS group; $$, p < 0.01, vs. 2% FBS + d-ECM group. P-ERK1/2, phospho-extracellular signal-regulated kinase1/2; ERK1/2, extracellular signal-regulated kinase1/2; PPARγ, peroxisome proliferators-activated receptor γ; C/EPBα, CCAAT enhancer-binding proteins

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