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PUBMED . NCBI . NLM . NIH . GOV {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Pubmed.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. CDN Services

We are analyzing https://pubmed.ncbi.nlm.nih.gov/23104876/.

Title:
Is p53 the long-sought molecular trigger for cyclophilin D-regulated mitochondrial permeability transition pore formation and necrosis? - PubMed
Description:
Is p53 the long-sought molecular trigger for cyclophilin D-regulated mitochondrial permeability transition pore formation and necrosis?
Website Age:
27 years and 8 months (reg. 1997-10-02).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Law & Government

Content Management System {πŸ“}

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

Custom-built

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

Traffic Estimate {πŸ“ˆ}

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

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


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Pubmed.ncbi.nlm.nih.gov Make Money? {πŸ’Έ}

We find it hard to spot revenue streams.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Pubmed.ncbi.nlm.nih.gov might have a hidden revenue stream, but it's not something we can detect.

Keywords {πŸ”}

pmid, doi, mitochondrial, permeability, transition, pore, pmc, cell, free, article, review, comment, articles, res, oct, epub, main, ncbi, similar, cited, resources, circresaha, cyclophilin, pubmed, death, nov, yang, hhs, page, content, homepage, navigation, search, full, text, publication, types, linkout, circ, trigger, necrosis, abstract, disclaimer, increased, cyclophilind, vulnerability, mar, redox, characterization, human,

Topics {βœ’οΈ}

main page content cyclophilin d-dependent control mitochondrial research long-sought molecular trigger 19094991 redox characterization permeability transition pore mitochondrial atp synthase necrotic cell death united states government novartis found symp compensated ventricular hypertrophy arch biochem biophys oxygen glucose deprivation/ oxygen glucose deprivation biochim biophys acta mol cell cardiol stress-induced opening similar articles cited /p53 signaling axis cell death increased vulnerability human cyclophilin targeting cyclophilin similar articles circ res hhs trigger necrosis cancer res neurochem res pubmed wordmark pubmed logo official website jason karchΒ 1 p53 opens vaseva av tsirka se moll um honokiol induces 17510419 increased expression intramitochondrial translocation cyclophilin young nt bourcier-lucas deschepper cf dietz kj tang dr oxygenation-induced zhao lp cardiac pathophysiology cardiovasc dis

Questions {❓}

  • Is p53 the long-sought molecular trigger for cyclophilin D-regulated mitochondrial permeability transition pore formation and necrosis?
  • Redox characterization of human cyclophilin D: identification of a new mammalian mitochondrial redox sensor?

External Links {πŸ”—}(31)

Analytics and Tracking {πŸ“Š}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • jQuery

CDN Services {πŸ“¦}

  • Ncbi

3.38s.