anti-CEBPA (CEBPA) Antikörper

Human CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. Concomitant WT1 mutations predict poor prognosis in acute myeloid leukemia patients with double mutant CEBPA.

2. These data suggest that down-regulation of C/EBPalpha by RBV leads to the reduction in GPAM expression, which contributes to the suppression of lipogenesis.

3. CEBPA supports vitamin D signaling concerning actions of the innate immune system, but uses the antagonism with PU.1 for suppressing possible overreactions of adaptive immunity.

4. FLT3-ITD was the most common mutated gene (16.2%, 42/259), followed by CEBPA (15.1%, 39/259), NRAS (14.7%, 38/259), and NPM1 (13.5%, 35/259). The results showed certain rules in the mutation profiling and concurrence of acute myeloid leukemia (AML) patients, which was related to the function classification of genes.

5. These results suggest that CEBPA(DM) cases with non-classic mutants may be functionally different from those with CEBPA(Classic-DM) mutants, and should not automatically be included in the same prognostic group

6. The prevalence of CSF3R mutations was high in AML patients with CEBPA(dm), which indicated a poor prognosis, and CSF3R mutations may be a new potential candidate for prognostically re-stratifying AML patients with CEBPA(dm).

7. these findings indicate that C/EBPalpha is required for Flt3(+) CLP maturation into preproB cells and then for proliferative Cebpa(int) B/myeloid preproB cells to progress to Cebpa(lo) B cell-restricted preproB cells and finally to Cebpa(neg) proB cells.

8. SaRNA accessory proteins may dictate efficacy of CEBPA-saRNA when used in a therapeutic context.

9. protein level of C/EBPalpha in CR patients with multiple myeloma was significantly higher than that in PR and relapsed patients by Western blot

10. our findings characterize ARID1A as a key tumor-suppressor gene in breast cancer through cooperation with CEBPalpha, and loss-of-function mutations of ARID1A activates UCA1.

11. PIWIL3 was also a target of CEBPA, forming a positive feedback loop in the growth regulation of glioma cells. Significantly, knockdown of OIP5-AS1 combined with over-expression of PIWIL3 and miR-367-3p resulted in tumor regression and extended survival in vivo.

12. C/EBPalpha overexpression does not change oncoprotein expression or globally displace these proteins from their binding sites. Instead, it upregulates a core set of common target genes important for myeloid differentiation and represses genes regulating leukemia maintenance.

13. during monocyte to macrophage differentiation, the endosomal/lysosomal proteolytic activity can be regulated by cystatin F whose expression is under the control of transcriptional factor C/EBP alpha.

14. We found 6 frame shift mutations, 1 missense mutation, 3 synonymous variants. The most common mutation was the c.487del G resulting p.Glu163Ser in 5 cases. Three patients carried CEBPA double mutations. CONCLUSION: The detected variants in this article seemed to be the first screening results of genes studied by NGS in pediatric acute leukemia patients.

15. The zinc finger, ZNF143, binds to the CCCAGCAG site in the CEBPA promoter.

16. The earliest steps of adult hepatocellular carcinoma and aggressive pediatric liver cancer have identical features that include conversion of the tumor suppressor C/EBPalpha into an oncogenic isoform, which further creates preneoplastic foci where hepatocytes dedifferentiate into cancer cells, giving rise to liver cancer

17. Data suggest that up-regulation of NPY inhibits proliferation of adipose-derived stem cells while promoting adipogenesis and up-regulating expression of white adipocyte biomarkers PPARG, CEBPA, CIDEC, and RIP140. (NPY = neuropeptide Y; PPARG = peroxisome proliferator activated receptor gamma; CIDEC = cell death-inducing DFFA-like effector C; RIP140 = nuclear receptor interacting protein 1)

18. Study identified for the first time that HNF4alpha and C/EBPalpha are important transcriptional regulators for FBP1 expression in human hepatoma HepG2 cells.

19. The presence of biallelic CEBPA mutations is a favourable prognostic feature in acute myeloid leukaemia.

20. C/EBP-alpha mediates anti-inflammatory effects in podocytes

Mouse (Murine) CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. Deletion of C/EBPalpha in Myeloid-derived suppressor cells enhanced the pro-angiogenic, immune suppressive and pro-tumorigenic behavior of these cells by upregulating the production of iNOS and arginase, as well as MMP-9 and VEGF

2. C/ebpalpha controls osteoclast terminal differentiation, activation, function, and postnatal bone homeostasis through direct regulation of Nfatc1 promoter region.

3. diminished expression of PU.1 or genetic deletion of C/EBPalpha in MLL-AF9 cells generates resistance of these leukemias to LSD1 inhibition. These findings reveal that pharmacologic inhibition of LSD1 represents a unique path to overcome the differentiation block in AML for therapeutic benefit.

4. results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPalpha and suppression of activation of NF-kappaB-driven proliferative inflammatory responses.

5. HBP1 knockdown leads to a significant reduction of C/EBPa expression, suggesting that HBP1-mediated C/EBPa expression may be needed for the termination of the cell cycle at the end of MCE for terminal differentiation

6. findings indicate that C/EBPalpha is a stronger inducer of osteoclast differentiation than c-Fos, partly via C/EBPalpha regulation by the RANK (535)IVVY(538) motif

7. The earliest steps of adult hepatocellular arcinoma and aggressive pediatric liver cancer have identical features that include conversion of the tumor suppressor C/EBPalpha into an oncogenic isoform, which further creates preneoplastic foci where hepatocytes dedifferentiate into cancer cells, giving rise to liver cancer

8. C/EBP-alpha mediates anti-inflammatory effects in podocytes

9. under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21.

10. the extracts dramatically attenuated the levels of adipogenic transcriptional factors, including CCAAT enhancer-binding protein alpha (C/EBPa), CCAAT enhancer-binding protein beta (C/EBPb), and gamma receptors by peroxisome proliferators (PPARg), during adipogenesis

11. shown that ectopic miR-155 expression and loss of C/EBPA expression in myeloid progenitor cells cooperate in transformation of HSPCs toward AML in the absence of FLT3-ITD

12. The Bach2-C/EBPbeta gene regulatory network pathway tunes multipotent progenitor commitment to myeloid and lymphoid lineages both under normal conditions and after infection.

13. Data demonstrate the importance of a controlled balance between C/EBPalpha and miR-182 for the maintenance of healthy granulopoiesis.

14. Functional characterization of C/EBPa and C/EBPb proteomes suggests they can regulate novel pathways.

15. results indicate that JMJD2B regulates PPARgamma and C/EBPalpha during adipogenesis

16. A single +42-kb enhancer is essential for CEBPA expression in myeloid cells only.

17. these data indicate that CycC activates adipogenesis in part by stimulating the transcriptional activity of C/EBPalpha.

18. Taken together, these findings demonstrate that artesunate inhibits adipogenesis in 3T3-L1 preadipoytes through the reduced expression and/or phosphorylation levels of C/EBP-alpha, PPAR-gamma, FAS, perilipin A, and STAT-3.

19. we show that SIX1 binds to adipogenic and brown marker genes and interacts with C/EBPa, C/EBPb and EBF2, suggesting their functional cooperation during adipogenesis.

20. these results indicate that C/EBPalpha functions throughout osteoclastogenesis as well as in Osteoclast function. This study provides additional understanding of the roles of C/EBPalpha in Osteoclast biology.

Zebrafish CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. a new role of Cebpalpha in embryonic myelopoiesis

2. C/ebpalpha plays a role in liver growth regulation via the p53 pathway.

3. Dnmt1 is required for hematopoietic stem and progenitor cells maintenance via cebpa regulation during definitive hematopoiesis in zebrafish

4. Data suggest that upregulation of 10-formyltetrahydrofolate dehydrogenase (FDH) involving CEBPalpha helps relieve embryonic oxidative stress induced by ethanol exposure.

5. Bmi1 acts immediately downstream of CCAAT enhancer binding protein-alpha to regulate the survival and self-renewal of hematopoietic stem cells and contribute to the erythropoietic dysplasia.

6. Results provide first evidence that sumoylation of Cebp-alpha (via SUMO1, SUMO2, and SUMO3) might contribute to cell fate decision of myelo-erythroid progenitor cells in intermediate cell mass during primitive [extramedullary] hematopoiesis.

7. An evolutionarily conserved PTEN-C/EBPalpha-CTNNA1 axis controls myeloid development and transformation.

Xenopus laevis CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. a C/EBP recognition sequence in the proximal promoter region of C/EBPalpha is essential for IL-6-mediated repression

Cow (Bovine) CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. These results suggest that the CEBPA gene is a strong candidate gene that affects carcass traits in Qinchuan cattle.

2. Expressions of C-EBPalpha and myostatin in muscles were higher in the concentrate-fed group than in the grass hay-fed group.

Pig (Porcine) CCAAT/enhancer Binding Protein (C/EBP), alpha (CEBPA) Interaktionspartner

1. C/EBPalpha is an essential regulatory factor for perilipin5 transcription and suggest that fasting stimulates perilipin5 transcription through influencing C/EBPalpha expression.

2. The differential expression of specific CEBPA/B isoforms observed in maturing follicles and CL may contribute to changes in follicular cell differentiation and increasing steroidogenic capacity.