Here's how DOI.ORG makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

DOI . ORG {}

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

We began analyzing https://elifesciences.org/articles/11612, but it redirected us to https://elifesciences.org/articles/11612. The analysis below is for the second page.

Title[redir]:
Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation | eLife
Description:
Macrophages are immune cells that are found in most of the tissues of the body. Exactly what the macrophages do depends on which tissue they are in, and the state of the tissue. For example, M2 macrophages can multiply in numbers, heal wounds or help to fight off parasites depending on the signals they receive from their environment. Conversely, when macrophages sense pathogens such as bacteria they can also become M1 macrophages, which produce inflammatory molecules that help kill the invading bacteria. As a macrophage transforms into a more specialized state, its metabolism – the set of chemical reactions the cell performs in order to survive and thrive – also changes. This shift appears to play an important role in activating the macrophages and determining how they’ll specialize. However, little is known about how metabolism exerts this control. The metabolism of a cell can be investigated in part by studying the molecules, or “metabolites”, that the cell produces. Covarrubias et al. studied what happens when unspecialized macrophages from mice were activated by a signaling molecule called IL-4. This signaling molecule causes the cells to become M2 macrophages, and the experiments revealed that IL-4 signaling controls the amount of a metabolite called acetyl-CoA in the cells. Acetyl-CoA can influence how the DNA of a gene is packaged in a cell, and thus affect whether a gene is switched on and “expressed” or not. Covarrubias et al. therefore also analyzed a major metabolic sensing pathway – the Akt-mTORC1 pathway – and showed how this pathway was able to act as a nutrient sensor for the macrophage and control the enzyme responsible for making acetyl-CoA. Therefore, the Akt-mTORC1 pathway can control the level of gene expression changes in the macrophages as a result of IL-4 signaling. The analysis showed that the increase in acetyl-CoA levels increases the expression of some of the genes that cause the M2 macrophages to change state and develop their specialist behaviors. However, only a subset of these genes – those that encode metabolically demanding activities such as immune cell trafficking – have their expression controlled in this way. Further studies are now needed to investigate whether other macrophage types use the same pathways to control their responses.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌟 Strong Traffic: 100k - 200k visitors per month


Based on our best estimate, this website will receive around 100,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

We're unsure how the site profits.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be cashing in, but we can't detect the method they're using.

Keywords {🔍}

figure, akt, activation, acly, genes, metabolic, google, scholar, macrophages, acetylation, data, signaling, control, analysis, accoa, histone, mtorc, supplement, levels, macrophage, aktmtorc, metabolism, gene, bmdms, cell, induction, activity, competing, interests, asset, article, amino, regulates, pathway, states, production, download, expression, inhibitor, phosphorylation, united, httpsdoiorgelife, aktdependent, open, state, role, nature, acid, protocol, authors,

Topics {✒️}

applying k-means clustering lc/ms-based metabolomics profiling hif-1α-mediated aerobic glycolysis ubc-creert2 raptorfl/fl mice stable isotope-labeled acyl-coenzyme ubiquitinc-creert2 raptorfl/fl mice [13c315n1]-acyl-coa internal standards akt-mtorc1 signaling regulates issam ben-sahra department 3h-deoxy-d-glucose tiffany polynne-stapornkul department lc/ms-based metabolomics o'neill krebs-ringer bicarbonate hepes 'neill la pi3k/akt signaling journal akt-mtorc1-acly axis rotenone increases lipid -oxidation akt-mtorc1 axis independent 2 mg/ml collagenase kinases tbk1-ikkɛ supports modulate akt-mtorc1 activity akt-mtorc1 signaling acts stat6-dependent luciferase reporter 5 mm 2-deoxy-d-glucose il-4-inducible acly phosphorylation heart 6-phosphofructo-2-kinase/fructose-2 akt-mediated acly activation transcription factor hif-1α stimulating gene-specific increases akt/acly-dependent rise gene-specific histone acetylation akt-mtorc1-acly pathway delta/delta ct method intracellular α-ketoglutarate maintains feeding/fasting experiments request examined gene-specific patterns β-oxidation inhibitor etomoxir feeding-induced atm polarization free ac-coa pool canonical jak-stat signaling bio-rad c1000 thermocycler rna-seq library construction acetyl-coa levels increases de novo lipogenesis akt-energy metabolism interactions nuclear-cytoplasmic pool relevant canonical jak-stat pathway metabolite called acetyl-coa mitochondrial ac-coa levels

Questions {❓}

  • How might Akt regulate increased histone acetylation in M2 macrophages?
  • How might Akt signaling regulate a subset of M2 genes?
  • Robey RBHay N (2009) Is akt the “warburg kinase”?
  • What about chemokines?
  • What is the teleological rationale for control of macrophage activation by Akt-mTORC1 signaling (and metabolism more generally)?
  • Why should some but not other components of the M2 response be regulated in this way?

Schema {🗺️}

ScholarlyArticle:
      context:https://schema.org
      mainEntityOfPage:
         type:WebPage
         id:https://elifesciences.org/articles/11612
      headline:Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation
      datePublished:2016-02-19
      author:
            type:Person
            name:Anthony J Covarrubias
            type:Person
            name:Halil Ibrahim Aksoylar
            type:Person
            name:Jiujiu Yu
            type:Person
            name:Nathaniel W Snyder
            type:Person
            name:Andrew J Worth
            type:Person
            name:Shankar S Iyer
            type:Person
            name:Jiawei Wang
            type:Person
            name:Issam Ben-Sahra
            type:Person
            name:Vanessa Byles
            type:Person
            name:Tiffany Polynne-Stapornkul
            type:Person
            name:Erika C Espinosa
            type:Person
            name:Dudley Lamming
            type:Person
            name:Brendan D Manning
            type:Person
            name:Yijing Zhang
            type:Person
            name:Ian A Blair
            type:Person
            name:Tiffany Horng
      publisher:
         type:Organization
         name:eLife Sciences Publications, Ltd
         logo:
            type:ImageObject
            url:https://elifesciences.org/assets/patterns/img/patterns/organisms/[email protected]
      keywords:
         macrophage metabolism
         macrophage activation
         immunometabolism
         akt
         acly
         mTORC1
      about:
         Cell Biology
         Immunology and Inflammation
      description:Interleukin 4 signaling co-opts the Akt-mTORC1-Acly pathway to couple metabolic input to the control of energetically demanding processes during macrophage M2 activation.
      isPartOf:
         type:Periodical
         name:eLife
         issn:2050-084X
WebPage:
      id:https://elifesciences.org/articles/11612
Person:
      name:Anthony J Covarrubias
      name:Halil Ibrahim Aksoylar
      name:Jiujiu Yu
      name:Nathaniel W Snyder
      name:Andrew J Worth
      name:Shankar S Iyer
      name:Jiawei Wang
      name:Issam Ben-Sahra
      name:Vanessa Byles
      name:Tiffany Polynne-Stapornkul
      name:Erika C Espinosa
      name:Dudley Lamming
      name:Brendan D Manning
      name:Yijing Zhang
      name:Ian A Blair
      name:Tiffany Horng
Organization:
      name:eLife Sciences Publications, Ltd
      logo:
         type:ImageObject
         url:https://elifesciences.org/assets/patterns/img/patterns/organisms/[email protected]
ImageObject:
      url:https://elifesciences.org/assets/patterns/img/patterns/organisms/[email protected]
Periodical:
      name:eLife
      issn:2050-084X

Social Networks {👍}(10)

External Links {🔗}(626)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Tag Manager

Libraries {📚}

  • Highcharts
  • Isotope
  • PhotoSwipe

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Cloudflare
  • Hypothes

4.14s.