Faculty Opinions recommendation of Genome-wide analysis of clustered Dorsal binding sites identifies putative target genes in the Drosophila embryo.

2002 ◽  
Author(s):  
Donald Rio
Keyword(s):  
Binding Sites ◽  
Target Genes ◽  
Drosophila Embryo ◽  
Genome Wide Analysis ◽  
Putative Target ◽  
Genome Wide

scholarly journals Genome-Wide Analysis of Binding Sites and Direct Target Genes of the Orphan Nuclear Receptor NR2F1/COUP-TFI

PLoS ONE ◽  
2010 ◽  
Vol 5 (1) ◽  
pp. e8910 ◽  
Author(s):  
Celina Montemayor ◽  
Oscar A. Montemayor ◽  
Alex Ridgeway ◽  
Feng Lin ◽  
David A. Wheeler ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Binding Sites ◽  
Target Genes ◽  
Orphan Nuclear Receptor ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Direct Target

scholarly journals Genome-wide analysis of repressor element 1 silencing transcription factor/neuron-restrictive silencing factor (REST/NRSF) target genes

2004 ◽  
Vol 101 (28) ◽  
pp. 10458-10463 ◽  
Author(s):  
A. W. Bruce ◽  
I. J. Donaldson ◽  
I. C. Wood ◽  
S. A. Yerbury ◽  
M. I. Sadowski ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Repressor Element

scholarly journals Genome-wide analysis of Nkx2.2 binding sites using ChIP-tag sequencing (ChIP-TS)

2007 ◽  
Vol 306 (1) ◽  
pp. 354
Author(s):  
Brad Hoffman ◽  
Daniel Kok ◽  
Joy Witzsche ◽  
Martin Hirst ◽  
Gordon Robertson ◽  
...  
Keyword(s):  
Binding Sites ◽  
Genome Wide Analysis ◽  
Genome Wide

scholarly journals Gene-specific mechanisms direct glucocorticoid-receptor-driven repression of inflammatory response genes in macrophages

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Maria A Sacta ◽  
Bowranigan Tharmalingam ◽  
Maddalena Coppo ◽  
David A Rollins ◽  
Dinesh K Deochand ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Binding Sites ◽  
De Novo ◽  
Elongation Factor ◽  
Myeloid Cell ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Mouse Macrophages ◽  
Underlying Mechanisms ◽  
Temporal Events

The glucocorticoid receptor (GR) potently represses macrophage-elicited inflammation, however, the underlying mechanisms remain obscure. Our genome-wide analysis in mouse macrophages reveals that pro-inflammatory paused genes, activated via global negative elongation factor (NELF) dissociation and RNA Polymerase (Pol)2 release from early elongation arrest, and non-paused genes, induced by de novo Pol2 recruitment, are equally susceptible to acute glucocorticoid repression. Moreover, in both cases the dominant mechanism involves rapid GR tethering to p65 at NF-kB-binding sites. Yet, specifically at paused genes, GR activation triggers widespread promoter accumulation of NELF, with myeloid cell-specific NELF deletion conferring glucocorticoid resistance. Conversely, at non-paused genes, GR attenuates the recruitment of p300 and histone acetylation, leading to a failure to assemble BRD4 and Mediator at promoters and enhancers, ultimately blocking Pol2 initiation. Thus, GR displays no preference for a specific pro-inflammatory gene class; however, it effects repression by targeting distinct temporal events and components of transcriptional machinery.

Sign in / Sign up

Export Citation Format

Share Document