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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. Social Networks
  9. External Links
  10. Analytics And Tracking
  11. Libraries
  12. Hosting Providers
  13. CDN Services

We began analyzing https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.106.681700, but it redirected us to https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.106.681700. The analysis below is for the second page.

Title[redir]:
Paraoxonase-2 Reduces Oxidative Stress in Vascular Cells and Decreases Endoplasmic Reticulum Stress–Induced Caspase Activation | Circulation
Description:
Background— In the vascular system, elevated levels of reactive oxygen species (ROS) produce oxidative stress and predispose to the development of atherosclerosis. Therefore, it is important to understand the systems producing and those scavenging vascular ROS. Here, we analyzed the ROS-reducing capability of paraoxonase-2 (PON2) in different vascular cells and its involvement in the endoplasmic reticulum stress pathway known as the unfolded protein response. Methods and Results— Quantitative real-time polymerase chain reaction and Western blotting revealed that PON2 is equally expressed in vascular cells and appears in 2 distinct glycosylated isoforms. By determining intracellular ROS, we show that overexpression of PON2 markedly reduced ROS, whereas its knockdown increased ROS levels significantly. Using microscopic and biochemical methods, we found PON2 mainly in the nuclear membrane and endoplasmic reticulum. Furthermore, PON2 expression was induced at both the promoter and protein levels by endoplasmic reticulum stress pathway unfolded protein response. This pathway may promote both apoptotic and survival mechanisms. Functionally, PON2 reduced unfolded protein response–accompanying oxidative stress and unfolded protein response–derived caspase activation. Conclusion— We suggest that PON2 represents an endogenous defense mechanism against vascular oxidative stress and unfolded protein response–induced cell death, thereby contributing to the prevention of atherosclerosis.

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

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?

🌍 Impressive Traffic: 500k - 1M visitors per month


Based on our best estimate, this website will receive around 600,019 visitors per month in the current month.
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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 {🔍}

pon, cells, figure, stress, ros, eahy, crossref, pubmed, vascular, google, scholar, cell, oxidative, protein, expression, paraoxonase, human, hours, response, shown, treated, caspase, western, upr, activity, analyzed, endothelial, ponisogfp, circulation, atherosclerosis, intracellular, proteins, apoptosis, smcs, tunicamycin, article, levels, control, endoplasmic, reticulum, cardiovascular, department, isoforms, gene, data, activation, results, view, disease, mrna,

Topics {✒️}

supplemental material file aha/asa scientific statements high-fat diet-fed rats pon2-iso1-gfp/-ha–overexpressing ea american heart association molecular biology reports transforming growth factor-β1 analyzing overexpressed pon2-iso1-gfp pon2-iso1-ha–overexpressing ea vascular nitric oxide pon2-iso1-gfp remained unchanged nitric oxide bioavailability apmap maintains endoplasmic-reticulum org/cgi/content/full/circulationaha 1 clinical perspective clinical perspective supplements download pdf nitric oxide depletion heart failure stroke oxidized low-density lipoprotein type ii diabetes overexpressing pon2-iso1-gfp glass-bottomed chamber slides ibrahim khalil al‐imran sites appears beneficial apolipoprotein e-deficient mice high-density lipoprotein fraction low-density lipoproteins accumulate reduces er stress endoplasmic reticulum stress references firefly luciferase gene putative pon2-iso1-gfp overexpressed pon2-iso1-gfp ��/− background conclusions acknowledgments 6 represent pon2-iso1-ha low density lipoprotein coronary heart disease author maximilian krüger include lipid/lipoprotein modifications substantial information funding financial support time-dependent fashion cell-based enzyme found glucose-regulated protein family main content advertisement signal mammalian glucose-regulated proteins

Social Networks {👍}(10)

External Links {🔗}(278)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Tag Manager

Libraries {📚}

  • Animate.css
  • Dropzone.js
  • Swiper
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
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  • mx3.zoho.eu

Name Servers:

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

CDN Services {📦}

  • Cookielaw

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