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NCBI . NLM . NIH . GOV {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Ncbi.nlm.nih.gov Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC5821458/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC5821458/. The analysis below is for the second page.

Title[redir]:
Gene-specific mechanisms direct glucocorticoid-receptor-driven repression of inflammatory response genes in macrophages - PMC
Description:
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 ...

Matching Content Categories {📚}

  • Science
  • Education
  • Books & Literature

Content Management System {📝}

What CMS is ncbi.nlm.nih.gov built with?

Custom-built

No common CMS systems were detected on Ncbi.nlm.nih.gov, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of ncbi.nlm.nih.gov audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,005 visitors per month in the current month.

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How Does Ncbi.nlm.nih.gov Make Money? {💸}

We find it hard to spot revenue streams.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Ncbi.nlm.nih.gov might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

genes, figure, doi, pol, lps, nelf, dex, bmdm, paused, binding, gene, repression, inflammatory, sites, peaks, brd, pubmed, google, scholar, article, pmc, occupancy, chipseq, nonpaused, recruitment, free, activation, lpsinduced, data, expression, analysis, response, tethering, promoters, transcription, nfκb, nelfb, mechanism, treatment, experiments, shown, treated, dexrepressed, supplement, nelfe, elongation, peak, transcriptional, elife, rna,

Topics {✒️}

crossed lysm-cre-het mice c57bl/6-derived lysm-cre mice p65/brd4-bound lps-induced enhancers lps-induced dex-insensitive genes lps-induced dex-repressed genes lps-induced dex-repressed genes funding statement lps-induced dex-insensitive transcripts lps-induced dex-repressed transcripts lps-induced dex-sensitive genes pmc beta search gc-sensitive pro-inflammatory genes bone marrow isolation nf-kb/rela binding motifs conserved n-terminal bromodomains acc=gse110279 acknowledgements centrally enriched nr3c-binding motifs lps+dex stimulation/repression discussed stimulus-responsive gene networks single chip-seq run de-novo recruitment thereof atp-dependent chromatin remodelers illumina-compatible sequencing library 1% methanol-free formaldehyde direct/indirect dna recruitment overlapped lps-induced peaks relative strand cross-correlations basal/uninduced cjun binding pro-inflammatory gene signature created ha-tagged versions alpha-mediated gene expression chip-seq peak calls evolutionarily conserved multi-protein qiagen rna-easy kit chip-seq datasets generated key relevant article performing chip-seq experiments random-primed cdna synthesis gov/geo/query/acc macrophage lps-induced transcriptome nf-κb gr-tethering sites candidate pro-inflammatory genes �tolerant’ lps-unresponsive state nuclear receptor-dependent repression exhibit promoter-proximal nelf lps-induced p65 targets preventing p-tefb recruitment candidate dex-repressed genes lps-dependent gene expression gr-mediated repression involves

Questions {❓}

  • 05 and >2 fold?
  • 11) Is the p65 binding regulated at the "paused" and "non-paused" inflammatory genes-associated enhancers/promoters by Dex?
  • 12) Are the histone acetylation and p300 binding are regulated at the "non-paused" inflammatory genes-associated promoters/enhancers in the absence of inflammatory stimuli by GR activation?
  • 13) How does NELF affect basal gene expression at paused inflammatory genes and intergenic enhancers?
  • 14) How the absence of NELF affects the recruitment of p65 and GR at paused genes?
  • 15) How Dex treatment affects NELF occupancy?
  • 7) On Figure 1E, are these GR peak categories overlap with p65 binding?
  • Does GR treatment prevent dismissal of NELF from paused promoters?
  • How do the authors know the relative contribution of p65 or other inflammatory transcription factors (AP1) to this "tethering"?
  • How does Dex pre-treatment followed by LPS stimulation affect gene expression at these loci?
  • How many genes do show similar NelfB dependency from the identified 201 liganded GR-repressed inflammatory genes?
  • Is there any relationship between these previous discoveries and the mechanisms of LPS+Dex stimulation/repression discussed in this manuscript?
  • Thus, do GR and NF-κB associate in order for GR to elicit its repressive effects?
  • What is the role of CDK9 on NF-κB and GR binding in the repression of inflammatory genes?
  • Non paused)?

Social Networks {👍}(6)

External Links {🔗}(144)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {📚}

  • jQuery
  • jQuery module (jquery-3.6.0)
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • nihcesxway.hub.nih.gov
  • nihcesxway2.hub.nih.gov
  • nihcesxway3.hub.nih.gov
  • nihcesxway4.hub.nih.gov
  • nihcesxway5.hub.nih.gov

Name Servers:

  • dns1-ncbi.ncbi.nlm.nih.gov
  • dns2-ncbi.ncbi.nlm.nih.gov
  • lhcns1.nlm.nih.gov
  • lhcns2.nlm.nih.gov

CDN Services {📦}

  • Ncbi

4.9s.