scholarly journals Blood Serum Alpha Fetoprotein Enhancer Binding Protein, a Tumor Suppressor, Decreases in Chronic HBV Hepatitis Patients as Hepatocellular Cancer Appears

2010 ◽  
Vol 28 (3) ◽  
pp. 125-135
Author(s):  
James N. Riggins ◽  
William Corey ◽  
Alfred N. Fonteh ◽  
Michael G. Harrington
Keyword(s):  
Tumor Suppressor ◽  
Binding Protein ◽  
Protein A ◽  
Hepatocellular Cancer ◽  
Alpha Fetoprotein ◽  
Reverse Phase ◽  
Enhancer Binding Protein ◽  
Hepatic Carcinogenesis ◽  
Serum Alpha Fetoprotein ◽  
Chronic Hbv

Chronic hepatitis increases the risk of hepatocellular carcinoma (HCC). To test whether circulating proteins reflect hepatic carcinogenesis, sera from patients and controls were albumin depleted, enriched for glycoproteins, digested with trypsin, and subjected to reverse phase chromatography and tandem mass spectrometry. Alpha-fetoprotein enhancer binding protein (AFPebp), a tumor suppressor, was repeatedly identified in sera from chronic HBV hepatitis patients. We independently identified and quantified AFPebp with a deuterated, phenylisocyanate-labeled synthetic peptide standard. Elevated AFPebp levels in sera from chronic HBV hepatitis patients decreased as cancer developed. These data suggest that rising AFPebp levels in chronic HBV hepatitis may be protective, while falling levels may contribute to HCC development.

A human alpha-fetoprotein enhancer-binding protein, ATBF1, contains four homeodomains and seventeen zinc fingers

1991 ◽  
Vol 11 (12) ◽  
pp. 6041-6049
Author(s):  
T Morinaga ◽  
H Yasuda ◽  
T Hashimoto ◽  
K Higashio ◽  
T Tamaoki
Keyword(s):  
Binding Protein ◽  
Zinc Fingers ◽  
Structural Features ◽  
Alpha Fetoprotein ◽  
Zinc Finger Motifs ◽  
Transcriptional Regulatory ◽  
Enhancer Binding Protein ◽  
Exact Function ◽  
Gene Enhancer ◽  
Number Of Segments

We have isolated a full-length cDNA encoding a protein (ATBF1) that binds to an AT-rich motif in the human alpha-fetoprotein gene enhancer. The amino acid sequence deduced from the cDNA revealed that this is the largest DNA-binding protein (306 kDa) known to date, containing four homeodomains, 17 zinc finger motifs, and a number of segments potentially involved in transcriptional regulation. Although the exact function of this protein has not been determined, these structural features suggest that ATBF1 plays a transcriptional regulatory role.

scholarly journals CCAAT enhancer binding protein β and hepatocyte nuclear factor 3β are necessary and sufficient to mediate dexamethasone-induced up-regulation of alpha2HS-glycoprotein/fetuin-A gene expression

2006 ◽  
Vol 36 (2) ◽  
pp. 261-277 ◽  
Author(s):  
Michael Wöltje ◽  
Beate Tschöke ◽  
Verena von Bülow ◽  
Ralf Westenfeld ◽  
Bernd Denecke ◽  
...  
Keyword(s):  
Serum Protein ◽  
Binding Protein ◽  
Protein A ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Tissue Remodelling ◽  
Mobility Shift ◽  
Fetuin A ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

Alpha2HS-glycoprotein/fetuin-A (Ahsg) is a serum protein preventing soft tissue calcification. In trauma and inflammation, Ahsg is down-regulated and therefore considered a negative acute phase protein. Enhancement of Ahsg expression as a protective serum protein is desirable in several diseases including tissue remodelling after trauma and infection, kidney and heart failure, and cancer. Using reporter gene assays in hepatoma cells combined with electrophoretic mobility shift assays we determined that dexamethasone up-regulates hepatic Ahsg. A steroid response unit at position −146/−119 within the mouse Ahsg promoter mediates the glucocorticoid-induced increase of Ahsg mRNA. It binds the hepatocyte nuclear factor 3β and CCAAT enhancer binding protein β (C/EBP-β). The up-regulation is mediated indirectly via glucocorticoid hormone-induced transcriptional up-regulation in C/EBP-β protein. A high degree of sequence identity in mouse, rat and human Ahsg promoters suggests that the promoter is similarly up-regulated by dexamethasone in all three species. Therefore, our findings suggest that glucocorticoids may be used to enhance the level of Ahsg protein circulating in serum.

scholarly journals Delta-interacting Protein A, a New Inhibitory Partner of CCAAT/Enhancer-binding Protein β, Implicated in Adipocyte Differentiation

2005 ◽  
Vol 280 (12) ◽  
pp. 11432-11438 ◽  
Author(s):  
Olivier Bezy ◽  
Christian Elabd ◽  
Olivia Cochet ◽  
Rasmus K. Petersen ◽  
Karsten Kristiansen ◽  
...  
Keyword(s):  
Adipocyte Differentiation ◽  
Binding Protein ◽  
Protein A ◽  
Interacting Protein ◽  
Enhancer Binding Protein ◽  
Ccaat Enhancer Binding Protein

scholarly journals Transcription Factor 21 Promotes Chicken Adipocyte Differentiation at Least in Part via Activating MAPK/JNK Signaling

Genes ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1971
Author(s):  
Xinyang Zhang ◽  
Bohan Cheng ◽  
Haixu Jiang ◽  
Chang Liu ◽  
Zhiping Cao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Line ◽  
Molecular Mechanisms ◽  
Binding Protein ◽  
Protein A ◽  
Peroxisome Proliferator ◽  
Jnk Pathway ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fatty Acid Binding ◽  
Enhancer Binding Protein

The molecular mechanisms of transcription factor 21 (TCF21) in regulating chicken adipogenesis remain unclear. Thus, the current study was designed to investigate the signaling pathway mediating the effect of TCF21 on chicken adipogenesis. Immortalized chicken preadipocytes cell line (ICP), a preadipocyte cell line stably overexpressing TCF21 (LV-TCF21) and a control preadipocyte cell line (LV-control) were used in the current study. We found that the phosphorylation of c-Jun N-terminal kinases (JNK) was significantly elevated in LV-TCF21 compared to LV-control. After treating ICP cells with a JNK inhibitor SP600125, the differentiation of ICP was inhibited, as evidenced by decreased accumulation of lipid droplets and reduced expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), adipocyte fatty acid binding protein (A-FABP), and lipoprotein lipase (LPL). Moreover, we found that the inhibition of JNK by SP600125 remarkably impaired the ability of TCF21 to drive adipogenesis. Taken together, our results suggest that TCF21 promotes the differentiation of adipocytes at least in part via activating MAPK/JNK pathway.

New B-lymphocyte-specific enhancer-binding protein

1989 ◽  
Vol 9 (1) ◽  
pp. 312-320
Author(s):  
A Dorn ◽  
C Benoist ◽  
D Mathis
Keyword(s):  
B Lymphocyte ◽  
Binding Protein ◽  
Protein A ◽  
The Other ◽  
Cross Linking ◽  
Recognition Sequence ◽  
Molecular Weights ◽  
Histocompatibility Complex ◽  
Enhancer Binding Protein ◽  
A Site

We report the discovery of a new B-lymphocyte-specific enhancer-binding protein. A series of gel retardation assays using fragments that scan the -2172 to -1180 region of the major histocompatibility complex class II gene E alpha reveal a site (W) that serves as the recognition sequence for two nuclear proteins, one B-cell restricted and the other ubiquitously occurring. Certain characteristics of the NF-W1 and NF-W2 pair recall the OTF-2/NF-A2 and OTF-1/NF-A1 pair that binds to the immunoglobulin octamer, but we demonstrate that the two protein pairs are distinguishable by several criteria. NF-W1 and NF-W2 interact differentially with their common GTTGCATC binding site, display a different affinity for it, and have molecular weights that differ by about 20,000. Yet, proteolysis experiments and cross-linking analyses indicate that the two W complexes show structural relatedness.

scholarly journals Tumor Suppressor HLJ1 Binds and Functionally Alters Nucleophosmin via Activating Enhancer Binding Protein 2  Complex Formation

2010 ◽  
Vol 70 (4) ◽  
pp. 1656-1667 ◽  
Author(s):  
T.-P. Chang ◽  
S.-L. Yu ◽  
S.-Y. Lin ◽  
Y.-J. Hsiao ◽  
G.-C. Chang ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Complex Formation ◽  
Binding Protein ◽  
Enhancer Binding Protein

scholarly journals CCAAT/Enhancer-Binding Protein Delta (C/EBPδ): A Previously Unrecognized Tumor Suppressor that Limits the Oncogenic Potential of Pancreatic Ductal Adenocarcinoma Cells

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2546
Author(s):  
Leonie Hartl ◽  
JanWillem Duitman ◽  
Hella L. Aberson ◽  
Kan Chen ◽  
Frederike Dijk ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Tumor Suppressor ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Binding Protein ◽  
Ductal Adenocarcinoma ◽  
Ductal Cells ◽  
Enhancer Binding Protein ◽  
Adenocarcinoma Cells ◽  
Ccaat Enhancer Binding Protein

CCAAT/enhancer-binding protein δ (C/EBPδ) is a transcription factor involved in growth arrest and differentiation, which has consequently been suggested to harbor tumor suppressive activities. However, C/EBPδ over-expression correlates with poor prognosis in glioblastoma and promotes genomic instability in cervical cancer, hinting at an oncogenic role of C/EBPδ in these contexts. Here, we explore the role of C/EBPδ in pancreatic cancer. We determined C/EBPδ expression in biopsies from pancreatic cancer patients using public gene-expression datasets and in-house tissue microarrays. We found that C/EBPδ is highly expressed in healthy pancreatic ductal cells but lost in pancreatic ductal adenocarcinoma. Furthermore, loss of C/EBPδ correlated with increased lymph node involvement and shorter overall survival in pancreatic ductal adenocarcinoma patients. In accordance with this, in vitro experiments showed reduced clonogenic capacity and proliferation of pancreatic ductal adenocarcinoma cells following C/EBPδ re-expression, concurrent with decreased sphere formation capacity in soft agar assays. We thus report a previously unrecognized but important tumor suppressor role of C/EBPδ in pancreatic ductal adenocarcinoma. This is of particular interest since only few tumor suppressors have been identified in the context of pancreatic cancer. Moreover, our findings suggest that restoration of C/EBPδ activity could hold therapeutic value in pancreatic ductal adenocarcinoma, although the latter claim needs to be substantiated in future studies.

Sign in / Sign up

Export Citation Format

Share Document