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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.
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.
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.
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.
The zinc finger, ZNF143, binds to the CCCAGCAG site in the CEBPA promoter.
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
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)
Study identified for the first time that HNF4alpha and C/EBPalpha are important transcriptional regulators for FBP1 expression in human hepatoma HepG2 cells.
The presence of biallelic CEBPA mutations is a favourable prognostic feature in acute myeloid leukaemia.
C/EBP-alpha mediates anti-inflammatory effects in podocytes
proteogenomics profiling study reveals that an activation of C/EBPalpha, along with the upregulation of its lipogenesis targets, accounts for lipid storage and acts as a hallmark of ARVC ( Arrhythmogenic right ventricular cardiomyopathy)
Taken together, the authors propose that the miR-939-Jmjd3 axis perturbs the accessibility of hepatitis B virus enhancer II/core promoter (En II) promoter to essential nuclear factors (C/EBPalpha and SWI/SNF complex) therefore leading to compromised viral RNA synthesis and hence restricted viral multiplication.
EBPA and RUNX1 are expressed at higher levels in patients with acute myeloid leukemia in comparison to healthy subjects
Integration of WGS-based fine-mapping and complementary epigenomic datasets provided evidence for causal mechanisms at several loci, including at a previously undiscovered basophil count-associated locus near the master hematopoietic transcription factor CEBPA The fine-mapped variant at this basophil count association near CEBPA overlapped an enhancer active in common myeloid progenitors and influenced its activity.
in our study on a large cohort of CEBPAmut AML patients, we found a high coincidence of GATA2mut, in particular within the subgroup of patients with CEBPAbi mutations
a decision analysis comparing allo-HCT vs chemotherapy in first complete remission for patients with cytogenetically intermediate-risk acute myeloid leukemia, depending on the presence or absence of FLT3-ITD), NPM1, and CEBPA mutations showed that allo-HCT was a favored postremission strategy in patients with FLT3-ITD, and chemotherapy was favored in patients with biallelic CEBPA mutations.
This is the first study providing evidence that the c.690G>T, p.(Thr230Thr) (rs34529039) polymorphism of the CEBPA gene, together with up-regulation of its mRNA expression, are negative factors worsening ovarian cancer outcome
CSF3R mutations co-occur with CEBPA mutations in pediatric acute myeloid leukemia.
While much is known about how C/EBPalpha orchestrates granulopoiesis, our understanding of molecular transformation events, the role(s) of cooperating mutations and clonal evolution during C/EBPalpha deregulation in leukemia remains elusive. In this review, we will summarize the latest research addressing these topics with special emphasis on CEBPA mutations
miR-182 is a strong regulator of C/EBPalpha. There is a regulatory loop between C/EBPalpha and miR-182. While C/EBPalpha blocks miR-182 expression by direct promoter binding during myeloid differentiation, enforced expression of miR-182 reduces C/EBPalpha protein level and impairs granulopoiesis in vitro and in vivo.
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
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
under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21.
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
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
The Bach2-C/EBPbeta gene regulatory network pathway tunes multipotent progenitor commitment to myeloid and lymphoid lineages both under normal conditions and after infection.
Data demonstrate the importance of a controlled balance between C/EBPalpha and miR-182 for the maintenance of healthy granulopoiesis.
Functional characterization of C/EBPa and C/EBPb proteomes suggests they can regulate novel pathways.
results indicate that JMJD2B regulates PPARgamma and C/EBPalpha during adipogenesis
A single +42-kb enhancer is essential for CEBPA expression in myeloid cells only.
these data indicate that CycC activates adipogenesis in part by stimulating the transcriptional activity of C/EBPalpha.
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.
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.
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.
the DNA sequences to which EVI1 binds at +35 and +37 kb and show that mutation of one of these releases Cebpa from EVI1-induced suppression.
The efficient repression of E2F dependent S-phase genes and the activation of differentiation genes reside in the balanced DNA binding capacity of C/EBP alpha.
Cebpa enhancers and silencers in a transcriptional model have roles in hematopoietic lineage specification
Data show that CCAAT-enhancer-binding protein-alpha (C/EBPalpha) directly regulates Kruppel-like factor 4 (Klf4) expression and increasing the levels of histone demethylase Lsd1 and transcription factor Brd4 in B cell.
The findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.
a new role of Cebpalpha in embryonic myelopoiesis
C/ebpalpha plays a role in liver growth regulation via the p53 pathway.
Dnmt1 is required for hematopoietic stem and progenitor cells maintenance via cebpa regulation during definitive hematopoiesis in zebrafish
Data suggest that upregulation of 10-formyltetrahydrofolate dehydrogenase (FDH) involving CEBPalpha helps relieve embryonic oxidative stress induced by ethanol exposure.
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.
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.
An evolutionarily conserved PTEN-C/EBPalpha-CTNNA1 axis controls myeloid development and transformation.
a C/EBP recognition sequence in the proximal promoter region of C/EBPalpha is essential for IL-6-mediated repression
These results suggest that the CEBPA gene is a strong candidate gene that affects carcass traits in Qinchuan cattle.
Expressions of C-EBPalpha and myostatin in muscles were higher in the concentrate-fed group than in the grass hay-fed group.
C/EBPalpha is an essential regulatory factor for perilipin5 transcription and suggest that fasting stimulates perilipin5 transcription through influencing C/EBPalpha expression.
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.
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. Also, the encoded protein can interact with CDK2 and CDK4, thereby inhibiting these kinases and causing growth arrest in cultured cells.
CCAAT/enhancer-binding protein alpha
, C/EBP alpha
, CAAT/enhancer-binding protein DNA-binding protein
, CAAT/enhancer-binding protein, DNA-binding protein
, CCAAT/enhancer binding protein, alpha
, c/EBP alpha
, CCAAT/enhancer binding protein alpha