Post-translational Control of ETS Transcription Factors: Detection of Modified Factors at Target Gene Promoters

2010 ◽  
pp. 279-289
Author(s):  
Li Li ◽  
Janice Saxton ◽  
Peter E. Shaw
Keyword(s):  
Transcription Factors ◽  
Translational Control ◽  
Target Gene ◽  
Gene Promoters ◽  
Ets Transcription Factors

scholarly journals Role of ETS Transcription Factors in the Hypoxia-Inducible Factor-2 Target Gene Selection

2006 ◽  
Vol 66 (11) ◽  
pp. 5641-5647 ◽  
Author(s):  
Olga Aprelikova ◽  
Matthew Wood ◽  
Sean Tackett ◽  
Gadisetti V.R. Chandramouli ◽  
J. Carl Barrett
Keyword(s):  
Transcription Factors ◽  
Target Gene ◽  
Gene Selection ◽  
Hypoxia Inducible Factor ◽  
Ets Transcription Factors

Nuclear hormone receptors PXR and CAR and metabolic diseases

2014 ◽  
Vol 19 (2) ◽  
Author(s):  
Li Mo ◽  
Jinhan He
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Thyroid Hormones ◽  
Nuclear Receptors ◽  
Target Gene ◽  
Hormone Receptors ◽  
Metabolic Diseases ◽  
Gene Promoters ◽  
Response Elements ◽  
Lipid Metabolites

AbstractNuclear receptors (NRs) belong to a superfamily of evolutionarily related DNA-binding transcription factors that can be activated by steroid and thyroid hormones, and other lipid metabolites. Ligand activated NRs can regulate target gene expression by binding to DNA response elements present in the target gene promoters. Through this regulation, NRs are broadly implicated in physiology and metabolism. In this chapter, we will focus on the xenobiotic receptors and their recently discovered functions in metabolic diseases.

scholarly journals Spi-1 and Fli-1 Directly Activate Common Target Genes Involved in Ribosome Biogenesis in Friend Erythroleukemic Cells

2009 ◽  
Vol 29 (10) ◽  
pp. 2852-2864 ◽  
Author(s):  
Gaëtan Juban ◽  
Guillaume Giraud ◽  
Boris Guyot ◽  
Stéphane Belin ◽  
Jean-Jacques Diaz ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Ribosome Biogenesis ◽  
Target Genes ◽  
Transcriptome Profiling ◽  
Gene Promoters ◽  
Ets Transcription Factors ◽  
Dna Binding Site ◽  
Friend Erythroleukemic Cells ◽  
Interfering Rna ◽  
Erythroleukemic Cells

ABSTRACT Spi-1 and Fli-1 are ETS transcription factors recurrently deregulated in mouse erythroleukemia induced by Friend viruses. Since they share the same core DNA binding site, we investigated whether they may contribute to erythroleukemia by common mechanisms. Using inducible knockdown, we demonstrated that Fli-1 contributes to proliferation, survival, and differentiation arrest of erythroleukemic cells harboring an activated fli-1 locus. Similarly, we used inducible Fli-1 knockdown and either hexamethylenebisacetamide (HMBA)- or small interfering RNA-mediated Spi-1 knockdown to investigate their respective contributions in erythroleukemic cells harboring an activated spi-1 locus. In these cells, simple or double knockdown of both Spi-1 and Fli-1 additively contributed to induce proliferation arrest and differentiation. Transcriptome profiling revealed that virtually all transcripts affected by both Fli-1 knockdown and HMBA are affected in an additive manner. Among these additively downregulated transcripts, more than 20% encode proteins involved in ribosome biogenesis, and conserved ETS binding sites are present in their gene promoters. Through chromatin immunoprecipitation, we demonstrated the association of Spi-1 and Fli-1 on these promoters in Friend erythroleukemic cells. These data lead us to propose that the oncogenicity of Spi-1, Fli-1, and possibly other ETS transcription factors may involve their ability to stimulate ribosome biogenesis.

scholarly journals The AML-associated K313 mutation enhances C/EBPα activity by leading to C/EBPα overexpression

2021 ◽  
Vol 12 (7) ◽  
Author(s):  
Ian Edward Gentle ◽  
Isabel Moelter ◽  
Mohamed Tarek Badr ◽  
Konstanze Döhner ◽  
Michael Lübbert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Culture ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Transcriptional Activity ◽  
Target Gene ◽  
Wild Type ◽  
Elevated Expression ◽  
Factor C ◽  
Acute Myeloid

AbstractMutations in the transcription factor C/EBPα are found in ~10% of all acute myeloid leukaemia (AML) cases but the contribution of these mutations to leukemogenesis is incompletely understood. We here use a mouse model of granulocyte progenitors expressing conditionally active HoxB8 to assess the cell biological and molecular activity of C/EBPα-mutations associated with human AML. Both N-terminal truncation and C-terminal AML-associated mutations of C/EBPα substantially altered differentiation of progenitors into mature neutrophils in cell culture. Closer analysis of the C/EBPα-K313-duplication showed expansion and prolonged survival of mutant C/EBPα-expressing granulocytes following adoptive transfer into mice. C/EBPα-protein containing the K313-mutation further showed strongly enhanced transcriptional activity compared with the wild-type protein at certain promoters. Analysis of differentially regulated genes in cells overexpressing C/EBPα-K313 indicates a strong correlation with genes regulated by C/EBPα. Analysis of transcription factor enrichment in the differentially regulated genes indicated a strong reliance of SPI1/PU.1, suggesting that despite reduced DNA binding, C/EBPα-K313 is active in regulating target gene expression and acts largely through a network of other transcription factors. Strikingly, the K313 mutation caused strongly elevated expression of C/EBPα-protein, which could also be seen in primary K313 mutated AML blasts, explaining the enhanced C/EBPα activity in K313-expressing cells.

scholarly journals Target Gene Specificity of E2F and Pocket Protein Family Members in Living Cells

2000 ◽  
Vol 20 (16) ◽  
pp. 5797-5807 ◽  
Author(s):  
Julie Wells ◽  
Kathryn E. Boyd ◽  
Christopher J. Fry ◽  
Stephanie M. Bartley ◽  
Peggy J. Farnham
Keyword(s):  
Cell Cycle ◽  
Target Gene ◽  
Target Genes ◽  
Protein Complexes ◽  
Current Model ◽  
Family Members ◽  
Living Cells ◽  
Gene Promoters ◽  
Pocket Protein ◽  
Protein Dna Interactions

ABSTRACT E2F-mediated transcription is thought to involve binding of an E2F-pocket protein complex to promoters in the G0 phase of the cell cycle and release of the pocket protein in late G1, followed by release of E2F in S phase. We have tested this model by monitoring protein-DNA interactions in living cells using a formaldehyde cross-linking and immunoprecipitation assay. We find that E2F target genes are bound by distinct E2F-pocket protein complexes which change as cells progress through the cell cycle. We also find that certain E2F target gene promoters are bound by pocket proteins when such promoters are transcriptionally active. Our data indicate that the current model applies only to certain E2F target genes and suggest that Rb family members may regulate transcription in both G0 and S phases. Finally, we find that a given promoter can be bound by one of several different E2F-pocket protein complexes at a given time in the cell cycle, suggesting that cell cycle-regulated transcription is a stochastic, not a predetermined, process.

scholarly journals Regulation of Poly(ADP-ribose) Polymerase-1-dependent Gene Expression through Promoter-directed Recruitment of a Nuclear NAD+ Synthase

2012 ◽  
Vol 287 (15) ◽  
pp. 12405-12416 ◽  
Author(s):  
Tong Zhang ◽  
Jhoanna G. Berrocal ◽  
Jie Yao ◽  
Michelle E. DuMond ◽  
Raga Krishnakumar ◽  
...  
Keyword(s):  
Enzymatic Activity ◽  
Target Gene ◽  
Target Genes ◽  
Enzymatic Activities ◽  
Gene Promoters ◽  
Protein Coding ◽  
Photon Excitation ◽  
Gene Sets ◽  
Cellular Compartments ◽  
Parp 1

NMNAT-1 and PARP-1, two key enzymes in the NAD+ metabolic pathway, localize to the nucleus where integration of their enzymatic activities has the potential to control a variety of nuclear processes. Using a variety of biochemical, molecular, cell-based, and genomic assays, we show that NMNAT-1 and PARP-1 physically and functionally interact at target gene promoters in MCF-7 cells. Specifically, we show that PARP-1 recruits NMNAT-1 to promoters where it produces NAD+ to support PARP-1 catalytic activity, but also enhances the enzymatic activity of PARP-1 independently of NAD+ production. Furthermore, using two-photon excitation microscopy, we show that NMNAT-1 catalyzes the production of NAD+ in a nuclear pool that may be distinct from other cellular compartments. In expression microarray experiments, depletion of NMNAT-1 or PARP-1 alters the expression of about 200 protein-coding genes each, with about 10% overlap between the two gene sets. NMNAT-1 enzymatic activity is required for PARP-1-dependent poly(ADP-ribosyl)ation at the promoters of commonly regulated target genes, as well as the expression of those target genes. Collectively, our studies link the enzymatic activities of NMNAT-1 and PARP-1 to the regulation of a set of common target genes through functional interactions at target gene promoters.

scholarly journals Differential regulation of neuronal nicotinic acetylcholine receptor subunit gene promoters by Brn-3 POU family transcription factors

1996 ◽  
Vol 317 (2) ◽  
pp. 419-423 ◽  
Author(s):  
Nathaniel G. N. MILTON ◽  
Alain BESSIS ◽  
Jean-Pierre CHANGEUX ◽  
David S. LATCHMAN
Keyword(s):  
Transcription Factors ◽  
Regulatory Region ◽  
Differential Regulation ◽  
Gene Promoters ◽  
The Novel ◽  
Receptor Subunit ◽  
Subunit Gene ◽  
Related Factors ◽  
Nicotinic Acetylcholine ◽  
Stimulation Of

The regulatory region of the neuronal nicotinic acetylcholine (nACh) receptor α2 subunit gene is activated by the Brn-3b POU family transcription factor but not by the closely related factors Brn-3a and Brn-3c. This pattern of regulation has not previously been observed for other neuronally expressed genes, several of which, such as those encoding α-internexin or SNAP-25, are activated by Brn-3a and Brn-3c but repressed by Brn-3b. The α3 nACh receptor subunit gene is also shown to be activated by Brn-3a but is repressed by Brn-3b and Brn-3c. In contrast, the Brn-3 POU family transcription factors have no effects on either the α7 or β4 nACh receptor subunit genes. The actions of Brn-3b on the α2 subunit are thus in contrast to the inhibitory actions of Brn-3b on several promoters that are activated by Brn-3a. The different actions of the Brn-3 POU factors on the range of nACh receptor genes tested suggests that the novel stimulation of the α2 subunit by Brn-3b is specific to this subunit and not a general feature of nACh receptor genes.

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