scholarly journals The ETS transcription factor ERF controls the exit from the naïve pluripotent state in a MAPK-dependent manner

2021 ◽  
Vol 7 (40) ◽  
Author(s):  
Maria Vega-Sendino ◽  
Teresa Olbrich ◽  
Desiree Tillo ◽  
Andy D. Tran ◽  
Catherine N. Domingo ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dependent Manner ◽  
Pluripotent State ◽  
Ets Transcription Factor

scholarly journals Dual function of the epithelial specific ets transcription factor, ELF3, in modulating differentiation

Oncogene ◽  
2000 ◽  
Vol 19 (15) ◽  
pp. 1941-1949 ◽  
Author(s):  
Felix H Brembeck ◽  
Oliver G Opitz ◽  
Towia A Libermann ◽  
Anil K Rustgi
Keyword(s):  
Transcription Factor ◽  
Dual Function ◽  
Ets Transcription Factor

scholarly journals Prostate-derived Ets transcription factor (PDEF) is a potential prognostic marker in patients with prostate cancer

The Prostate ◽  
2011 ◽  
Vol 71 (11) ◽  
pp. 1178-1188 ◽  
Author(s):  
Ali Ghadersohi ◽  
Satish Sharma ◽  
Shaozeng Zhang ◽  
Rami G. Azrak ◽  
Gregory E. Wilding ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Prognostic Marker ◽  
Ets Transcription Factor

scholarly journals Ligand-dependent repression of the erythroid transcription factor GATA-1 by the estrogen receptor.

1995 ◽  
Vol 15 (6) ◽  
pp. 3147-3153 ◽  
Author(s):  
G A Blobel ◽  
C A Sieff ◽  
S H Orkin
Keyword(s):  
Bone Marrow ◽  
Estrogen Receptor ◽  
Transcription Factor ◽  
Progenitor Cells ◽  
Erythroid Cell ◽  
High Dose ◽  
Dependent Manner ◽  
Erythroid Progenitor ◽  
Erythroid Progenitor Cells

High-dose estrogen administration induces anemia in mammals. In chickens, estrogens stimulate outgrowth of bone marrow-derived erythroid progenitor cells and delay their maturation. This delay is associated with down-regulation of many erythroid cell-specific genes, including alpha- and beta-globin, band 3, band 4.1, and the erythroid cell-specific histone H5. We show here that estrogens also reduce the number of erythroid progenitor cells in primary human bone marrow cultures. To address potential mechanisms by which estrogens suppress erythropoiesis, we have examined their effects on GATA-1, an erythroid transcription factor that participates in the regulation of the majority of erythroid cell-specific genes and is necessary for full maturation of erythrocytes. We demonstrate that the transcriptional activity of GATA-1 is strongly repressed by the estrogen receptor (ER) in a ligand-dependent manner and that this repression is reversible in the presence of 4-hydroxytamoxifen. ER-mediated repression of GATA-1 activity occurs on an artificial promoter containing a single GATA-binding site, as well as in the context of an intact promoter which is normally regulated by GATA-1. GATA-1 and ER bind to each other in vitro in the absence of DNA. In coimmunoprecipitation experiments using transfected COS cells, GATA-1 and ER associate in a ligand-dependent manner. Mapping experiments indicate that GATA-1 and the ER form at least two contacts, which involve the finger region and the N-terminal activation domain of GATA-1. We speculate that estrogens exert effects on erythropoiesis by modulating GATA-1 activity through protein-protein interaction with the ER. Interference with GATA-binding proteins may be one mechanism by which steroid hormones modulate cellular differentiation.

ERP, a new member of the ets transcription factor/oncoprotein family: cloning, characterization, and differential expression during B-lymphocyte development

1994 ◽  
Vol 14 (5) ◽  
pp. 3292-3309
Author(s):  
M Lopez ◽  
P Oettgen ◽  
Y Akbarali ◽  
U Dendorfer ◽  
T A Libermann
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Gene Family ◽  
B Cell ◽  
Binding Sites ◽  
B Lymphocyte ◽  
Striking Similarity ◽  
Lymphocyte Development ◽  
B Lymphocyte Development ◽  
Ets Transcription Factor

The ets gene family encodes a group of proteins which function as transcription factors under physiological conditions and, if aberrantly expressed, can cause cellular transformation. We have recently identified two regulatory elements in the murine immunoglobulin heavy-chain (IgH) enhancer, pi and microB, which exhibit striking similarity to binding sites for ets-related proteins. To identify ets-related transcriptional regulators expressed in pre-B lymphocytes that may interact with either the pi or the microB site, we have used a PCR approach with degenerate oligonucleotides encoding conserved sequences in all members of the ets family. We have cloned the gene for a new ets-related transcription factor, ERP (ets-related protein), from the murine pre-B cell line BASC 6C2 and from mouse lung tissue. The ERP protein contains a region of high homology with the ETS DNA-binding domain common to all members of the ets transcription factor/oncoprotein family. Three additional smaller regions show homology to the ELK-1 and SAP-1 genes, a subgroup of the ets gene family that interacts with the serum response factor. Full-length ERP expresses only negligible DNA-binding activity by itself. Removal of the carboxy terminus enables ERP to interact with a variety of ets-binding sites including the E74 site, the IgH enhancer pi site, and the lck promoter ets site, suggesting a carboxy-terminal negative regulatory domain. At least three ERP-related transcripts are expressed in a variety of tissues. However, within the B-cell lineage, ERP is highly expressed primarily at early stages of B-lymphocyte development, and expression declines drastically upon B-cell maturation, correlating with the enhancer activity of the IgH pi site. These data suggest that ERP might play a role in B-cell development and in IgH gene regulation.

scholarly journals Hypertonicity-induced phosphorylation and nuclear localization of the transcription factor TonEBP

2001 ◽  
Vol 280 (2) ◽  
pp. C248-C253 ◽  
Author(s):  
Stephen C. Dahl ◽  
Joseph S. Handler ◽  
H. Moo Kwon
Keyword(s):  
Transcription Factor ◽  
Nuclear Localization ◽  
Kinase Inhibitors ◽  
Dependent Manner ◽  
Binding Assays ◽  
P38 Inhibitor ◽  
Vitro Binding ◽  
Compatible Osmolytes

The accumulation of compatible osmolytes during osmotic stress is observed in virtually all organisms. In mammals, the hypertonicity-induced expression of osmolyte transporters and synthetic enzymes is conferred by the presence of upstream tonicity-responsive enhancer (TonE) sequences. Recently, we described the cloning and initial characterization of TonE-binding protein (TonEBP), a transcription factor that translocates to the nucleus and associates with TonE sequences in a tonicity-dependent manner. We now report that hypertonicity induces an increase in TonEBP phosphorylation that temporally correlates with increased nuclear localization of the molecule. TonEBP phosphorylation is not affected by a number of kinase inhibitors, including the p38 inhibitor SB-203580. In addition, in vitro binding assays show that the association of TonEBP with TonE sequences is not affected by phosphorylation. Thus TonEBP phosphorylation is an early step in the response of cells to hypertonicity and may be required for nuclear import or retention.

scholarly journals ETV5 regulates hepatic fatty acid metabolism through PPAR signaling pathway

2020 ◽  
Author(s):  
Ada Admin ◽  
Zhuo Mao ◽  
Mingji Feng ◽  
Zhuoran Li ◽  
Minsi Zhou ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Association Studies ◽  
Sequencing Analysis ◽  
Dependent Manner ◽  
Alcoholic Fatty Liver ◽  
Hepatic Fatty Acid ◽  
Ppar Signaling

ETV5 is an ETS transcription factor which has been associated with obesity in genomic association studies. However, little is known about the role of ETV5 in hepatic lipid metabolism and non-alcoholic fatty liver disease (NAFLD). In the present study, we found that ETV5 protein expression was increased in diet- and genetic-induced steatotic liver. ETV5 responded to the nutrient status in an mTORC1 dependent manner and in turn regulated mTORC1 activity. Both viral-mediated and genetic depletion of ETV5 in mice led to increased lipid accumulation in the liver. RNA sequencing analysis revealed that PPAR signaling and fatty acid degradation/metabolism pathways were significantly downregulated in ETV5 deficient hepatocytes <i>in vivo</i> and <i>in vitro. </i>Mechanistically, ETV5 could bind to the PPRE region of PPAR downstream genes and enhance its transactivity. Collectively, our study identifies ETV5 as a novel transcription factor for the regulation of hepatic fatty acid metabolism which is required for the optimal β oxidation process. ETV5 may provide a therapeutic target for the treatment of hepatic steatosis.<br>

scholarly journals SUMO conjugation susceptibility of Akt/protein kinase B affects the expression of the pluripotency transcription factor Nanog in embryonic stem cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254447
Author(s):  
Marcos Francia ◽  
Martin Stortz ◽  
Camila Vazquez Echegaray ◽  
Camila Oses ◽  
Paula Verneri ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Es Cells ◽  
Embryonic Stem ◽  
Dependent Manner ◽  
Cellular Functions ◽  
Cellular Processes ◽  
Sumo Conjugation ◽  
Heterologous System ◽  
Canonical Pathways ◽  
The Impact

Akt/PKB is a kinase involved in the regulation of a wide variety of cell processes. Its activity is modulated by diverse post-translational modifications (PTMs). Particularly, conjugation of the small ubiquitin-related modifier (SUMO) to this kinase impacts on multiple cellular functions, such as proliferation and splicing. In embryonic stem (ES) cells, this kinase is key for pluripotency maintenance. Among other functions, Akt is known to promote the expression of Nanog, a central pluripotency transcription factor (TF). However, the relevance of this specific PTM of Akt has not been previously analyzed in this context. In this work, we study the effect of Akt1 variants with differential SUMOylation susceptibility on the expression of Nanog. Our results demonstrate that both, the Akt1 capability of being modified by SUMO conjugation and a functional SUMO conjugase activity are required to induce Nanog gene expression. Likewise, we found that the common oncogenic E17K Akt1 mutant affected Nanog expression in ES cells also in a SUMOylatability dependent manner. Interestingly, this outcome takes places in ES cells but not in a non-pluripotent heterologous system, suggesting the presence of a crucial factor for this induction in ES cells. Remarkably, the two major candidate factors to mediate this induction, GSK3-β and Tbx3, are non-essential players of this effect, suggesting a complex mechanism probably involving non-canonical pathways. Furthermore, we found that Akt1 subcellular distribution does not depend on its SUMOylatability, indicating that Akt localization has no influence on the effect on Nanog, and that besides the membrane localization of E17K Akt mutant, SUMOylation is also required for its hyperactivity. Our results highlight the impact of SUMO conjugation in the function of a kinase relevant for a plethora of cellular processes, including the control of a key pluripotency TF.

scholarly journals Molecular-genetic mechanisms of regulation of dihydroflavonol reductase and transcription factor Hy5 by exogenous 5-aminolevulinic acid in winter rape plants

2020 ◽  
Vol 64 (3) ◽  
pp. 317-324
Author(s):  
N. G. Averina ◽  
H. V. Yemelyanava ◽  
T. G. Kaliaha ◽  
S. M. Savina
Keyword(s):  
Transcription Factor ◽  
Light Intensity ◽  
Aminolevulinic Acid ◽  
Molecular Level ◽  
Molecular Genetic ◽  
High Light Intensity ◽  
Dependent Manner ◽  
Winter Rape ◽  
Additional Increase ◽  
Stimulation Of

The effect of exogenous 5-aminolevulinic acid (ALA) on the activity of dihydroflavonol-4-reductase (DFR), the expression of the dfr gene and the hy5 gene of the transcription factor Hy5 and the light effect of different intensities in combination with the ALA action on the accumulation of anthocyanins in cotyledonous leaves of winter rape (Brassica napus L.) were studied. It was shown that the stimulation of the accumulation of anthocyanins under the exogenous ALA action at the molecular level was provided by increasing the expression level of the dfr and hy5 genes and the activity of the DFR enzyme. Increasing the light intensity from 40.5 to 66.2 μmol photons/m2·s enhanced the ability of plants to accumulate anthocyanins on average by 35 %. The ALA action at concentrations of 50, 100, 150 and 200 mg/L led to an additional increase in the accumulation of anthocyanins at the two used levels of illumination, and in a dose-dependent manner. The stimulating effect of ALA under high light intensity was much higher than in the case of lower illumination. Thus, the stimulation of the anthocyanin accumulation under illumination of 40.5 μmol photons/m2·s was 106 % when using 50 mg/L ALA, 165 % – when using 100 mg/L ALA, 222 % – in the case of 150 mg/L ALA and 350 % – under the action of 200 mg/L ALA compared with light control without of ALA treatment. At an illumination of 66.2 μmol photons/m2·s, these indicators were 164, 262, 359 and 583 % respectively. Thus, it was demonstrated that the stimulation of the accumulation of anthocyanins under the action of ALA in winter rape plants was due to its positive effect on the transcription of the dfr and hy5 genes at the molecular level.

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