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  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. Social Networks
  10. External Links
  11. Analytics And Tracking
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We began analyzing https://www.molbiolcell.org/doi/10.1091/mbc.e02-09-0621, but it redirected us to https://www.molbiolcell.org/doi/10.1091/mbc.e02-09-0621. The analysis below is for the second page.

Title[redir]:
Biphasic Estradiol-induced AKT Phosphorylation Is Modulated by PTEN via MAP Kinase in HepG2 Cells | Molecular Biology of the Cell
Description:
We reported previously in HepG2 cells that estradiol induces cell cycle progression throughout the G1–S transition by the parallel stimulation of both PKC-α and ERK signaling molecules. The analysis of the cyclin D1 gene expression showed that only the MAP kinase pathway was involved. Here, the presence of rapid/nongenomic, estradiol-regulated, PI3K/AKT signal transduction pathway, its modulation by the levels of the tumor suppressor PTEN, its cross-talk with the ERK pathway, and its involvement in DNA synthesis and cyclin D1 gene promoter activity have all been studied in HepG2 cells. 17β-Estradiol induced the rapid and biphasic phosphorylation of AKT. These phosphorylations were independent of each other, being the first wave of activation independent of the estrogen receptor (ER), whereas the second was dependent on ER. Both activations were dependent on PI3K activity; furthermore, the ERK pathway modulated AKT phosphorylation by acting on the PTEN levels. The results showed that the PI3K pathway, as well as ER, were strongly involved in both G1–S progression and cyclin D1 promoter activity by acting on its proximal region (-254 base pairs). These data indicate that in HepG2 cells, different rapid/nongenomic estradiol-induced signal transduction pathways modulate the multiple steps of G1–S phase transition.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

Content Management System {📝}

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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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 75,489,999 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We can't see how the site brings in money.

Not all websites are made for profit; some exist to inform or educate users. Or any other reason why people make websites. And this might be the case. Doi.org could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

cells, google, scholar, cyclin, medline, cell, einduced, akt, phosphorylation, pik, crossref, pten, hepg, activation, promoter, kinase, min, estrogen, pathway, levels, activity, dna, figure, inhibitors, marino, synthesis, protein, erk, gene, membrane, map, role, pip, ici, cancer, receptor, cycle, progression, signaling, stimulation, expression, tumor, rapid, wortmannin, mol, effects, test, human, pathways, transcription,

Topics {✒️}

e2-induced rapid/nongenomic mechanisms e2-induced rapid/nongenomic phosphorylation serine/threonine kinase akt/pkb pi3-kinase/akt signalling pathway mitogen-activated protein kinase plasma membrane–nonpermeating e2–bsa ligand-inducible transcriptional enhancer monoclonal anti–phospho-akt antibody prevent e2-induced reduction gibco-brl life technology e2-induced pi3k/akt activation estradiol-induced ip3 mediate e2-induced nongenomic actions allowing e2-induced phosphorylation map kinase/erk pathways e2-regulated mitogenesis starts e2-induced map kinase rapid/nongenomic signaling molecules phosphoinositide 3-kinase/akt pathway e2-induced dna synthesis filtrate contained e2–bsa e2-induced erk phosphorylation e2-induced akt phosphorylation p36d1-p34cdk4 complex activation estradiol-induced pi3k pathway pure anti–estrogen receptor e2-induced cell proliferation gc-rich sp1 sites cdp-star chemiluminescence reagent γ-adrenergic membrane er e2-induced thymidine incorporation e2-induced erk activation estrogen receptor-α detected ligand-dependent trans-activation e2-induced target genes anti–β-actin antibodies cyclin d1 gene anti–β-actin antibody e2-induced pkc-α phosphatidylinositol 3-kinase/akt pathway fetal calf serum cyclin d1 transcription cyclin d1 promoter multiple cis-elements er-dependent erk phosphorylation er-dependent akt phosphorylation inducible regulatory elements ere-dependent transcriptional activity cyclin d1 induction cyclin d1 protein

Questions {❓}

  • PI3-kinase inhibition: a target for drug development?
  • The plasma membrane estrogen receptor: nuclear or unclear?

Social Networks {👍}(2)

External Links {🔗}(293)

Analytics and Tracking {📊}

  • Google Analytics
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Libraries {📚}

  • Dropzone.js
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Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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Name Servers:

  • josh.ns.cloudflare.com
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CDN Services {📦}

  • Pbgrd

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