产品: C/EBP alpha 抗体
货号: AF6333
描述: Rabbit polyclonal antibody to C/EBP alpha
应用: WB IHC IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Bovine
分子量: 30,43kDa; 38kD(Calculated).
蛋白号: P49715
RRID: AB_2835189

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   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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产品描述

来源:
Rabbit
应用:
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.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human,Mouse,Rat
预测:
Pig(100%), Bovine(100%)
克隆:
Polyclonal
特异性:
C/EBP alpha Antibody detects endogenous levels of total C/EBP alpha.
RRID:
AB_2835189
引用格式: Affinity Biosciences Cat# AF6333, RRID:AB_2835189.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
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.
别名:

展开/折叠

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;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
描述:
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.
序列:
MESADFYEAEPRPPMSSHLQSPPHAPSSAAFGFPRGAGPAQPPAPPAAPEPLGGICEHETSIDISAYIDPAAFNDEFLADLFQHSRQQEKAKAAVGPTGGGGGGDFDYPGAPAGPGGAVMPGGAHGPPPGYGCAAAGYLDGRLEPLYERVGAPALRPLVIKQEPREEDEAKQLALAGLFPYQPPPPPPPSHPHPHPPPAHLAAPHLQFQIAHCGQTTMHLQPGHPTPPPTPVPSPHPAPALGAAGLPGPGSALKGLGAAHPDLRASGGSGAGKAKKSVDKNSNEYRVRRERNNIAVRKSRDKAKQRNVETQQKVLELTSDNDRLRKRVEQLSRELDTLRGIFRQLPESSLVKAMGNCA

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Pig
100
Bovine
100
Horse
0
Sheep
0
Dog
0
Xenopus
0
Zebrafish
0
Chicken
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P49715 作为底物

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

研究背景

功能:

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.

翻译修饰:

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.

细胞定位:

Nucleus.

Nucleus>Nucleolus.

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

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.

蛋白家族:

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

Belongs to the bZIP family. C/EBP subfamily.

研究领域

· 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)

文献引用

1). Adipose specific aptamer adipo-8 recognizes and interacts with APMAP to ameliorates fat deposition in vitro and in vivo. LIFE SCIENCES (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 (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 (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 [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 (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 (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). 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 (PubMed: 32814091) [IF=3.8]

8). 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 (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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