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

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

DOI . ORG {}

Detected CMS Systems:

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

We began analyzing https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1006355, but it redirected us to https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1006355. The analysis below is for the second page.

Title[redir]:
No title found...
Description:
Author Summary Mitochondrial transfer tRNA (mt-tRNA) contains a variety of chemical modifications that are introduced post-transcriptionally. Three mt-tRNAs for Lys, Gln and Glu contain 5-taurinomethyl-2-thiouridine (τm5s2U) in their anticodons. It is known that the loss of 2-thiolation of τm5s2U is strongly associated with the development of reversible infantile liver failure (RILF) because pathogenic mutations of RILF were found in the MTU1 gene, which encodes an enzyme responsible for the 2-thiolation of τm5s2U. However, the molecular mechanism underlying RILF pathogenesis associated with a lack of MTU1 remains elusive. To understand the physiological function of MTU1 and its association with liver failure, we generated liver-specific Mtu1-deficient (Mtu1LKO) mice. Mtu1 deficiency abolished 2-thiouridine formation in the three mt-tRNAs. Loss of the 2-thiouridine modification resulted in a marked impairment of mitochondrial translation and abnormal mitochondrial structure. Consequently, the Mtu1LKO mice exhibited liver injury, which resembles the symptoms of RILF patients. Furthermore, mitochondrial dysfunction in Mtu1LKO mice induced mitochondrial biogenesis and suppressed oxidative stress. These findings elucidate the cellular and physiological functions of Mtu1 and provide a mouse model for understanding RILF pathogenesis.

Matching Content Categories {📚}

  • Pets
  • Science
  • Education

Content Management System {📝}

What CMS is doi.org built with?


Doi.org is based on WORDPRESS. But there are also traces of other content systems on the page (hubspot).

Traffic Estimate {📈}

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

🌌 Gigantic Traffic: 2M - 5M visitors per month


Based on our best estimate, this website will receive around 4,026,036 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Doi.org Make Money? {💸}

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. Doi.org might be earning cash quietly, but we haven't detected the monetization method.

Wordpress Themes and Plugins {🎨}

What WordPress theme does this site use?

It is strange but we were not able to detect any theme on the page.

What WordPress plugins does this website use?

It is strange but we were not able to detect any plugins on the page.

Keywords {🔍}

mice, mitochondrial, mtu, mtulko, fig, liver, translation, levels, article, hepatocytes, view, google, scholar, pmid, pubmedncbi, rilf, lko, modification, flox, livers, mtudeficient, patients, deficiency, stress, knockout, modifications, exhibited, oxidative, image, mtuflox, mutations, results, respiratory, plos, weekold, control, injury, mttrnas, trnas, molecular, dysfunction, protein, examined, expression, representative, infantile, suzuki, gene, mouse, genes,

Topics {✒️}

plos genet 12 cookies plos biology current genetics 2005 generated liver-specific mtu1-deficient muscle-specific mtu1-deificient mice hepatocyte-specific mtu1 knockout animals obtained generated liver-specific knockout mtu1-mediated thiouridine formation mtu1-mediated 2-thiouridine formation fully modified mt-trnas liver-bone endocrine relay murine models mt-trna-modifying enzymes von kleist-retzow jc oxidative stress-related metabolites glucose-6-phosphatase catalytic subunit original author human mitochondrial diseases cdk5rap1-mediated 2-methylthio modification primerscript rt-pcr kit individual complex activity mtu1-mediated mitochondrial translation respiratory complex activities modified view infantile reversible cytochrome mitochondrial mt-tf variant trna-modifying enzymes mtu1-deficient hepatocytes compared mtu1-mediated s2 modification mitochondrial aspartyl-trna synthetase high-density lipoprotein cholesterol partially s2-modified mtu1-deficient primary hepatocytes life-threatening condition characterized blood vessel networks induced liver injury adult mtu1-deficient mice exhibited normal translation mitochondrial diseases complex iii suppressed oxidative stress liver injury characterized catastrophic liver failure mtdna-encoded mitochondrial genes mitochondrial protein translation selected metabolism-related genes aberrant structures magnified biosynthesis

Questions {❓}

  • Why is Mtu1-mediated s2 modification crucial for mitochondrial translation?

Social Networks {👍}(3)

External Links {🔗}(228)

Analytics and Tracking {📊}

  • Facebook Pixel
  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager
  • Google Universal Analytics
  • HubSpot

Libraries {📚}

  • Foundation
  • jQuery
  • Leaflet
  • Lightbox
  • Modernizr
  • Moment.js
  • Underscore.js
  • Video.js
  • Vue.js
  • Zoom.js

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
  • Crossref

5.83s.