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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. Schema
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
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We began analyzing https://www.nature.com/articles/1204288, but it redirected us to https://www.nature.com/articles/1204288. The analysis below is for the second page.

Title[redir]:
Endoplasmic reticulum localized Bcl-2 prevents apoptosis when redistribution of cytochrome c is a late event | Oncogene
Description:
The disruption of mitochondrial function is a key component of apoptosis in most cell types. Localization of Bcl-2 to the outer mitochondrial and endoplasmic reticulum membranes is consistent with a role in the inhibition of many forms of apoptosis. In Rat-1 cells, a Bcl-2 mutant targeted exclusively to the endoplasmic reticulum (Bcl-cb5) was effective at inhibiting apoptosis induced by serum starvation/myc, or ceramide but not apoptosis induced by etoposide. The former conditions cause a decrease in mitochondrial transmembrane potential (Δψm) as an early event that precedes the release of cytochrome c from mitochondria. By contrast, when cells are exposed to etoposide, a situation in which cytochrome c release and membrane localization of the pro-apoptotic protein Bax precede loss of Δψm, wild type Bcl-2 but not Bcl-cb5 prevents apoptosis. Therefore, Bcl-2 functions in spatially distinct pathways of apoptosis distinguished by the order of cytochrome c release and loss of Δψm.

Matching Content Categories {📚}

  • Social Networks
  • Telecommunications
  • Animals & Wildlife

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?

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


Based on our best estimate, this website will receive around 80,479,999 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 has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

nature, kroemer, bcl, apoptosis, zamzami, cell, oncogene, article, access, biol, med, susin, content, leber, exp, cookies, cytochrome, andrews, mitochondrial, embo, privacy, endoplasmic, reticulum, zhu, penn, castedo, research, canada, data, open, chem, green, marchetti, wang, advertising, information, journal, subscribe, prevents, event, annis, brian, cells, δψm, release, loss, institution, buy, proteins, bossywetzel,

Topics {✒️}

nature portfolio permissions reprints privacy policy medical research council author information authors advertising 1997 nature med social media 1998 nature 391 2000 nature 403 1997 nature 386 1999 nature 399 nature bcl-cb5 prevents apoptosis personal data data protection permissions springerlink instant access brian leber & david endoplasmic reticulum membranes mitochondrial apoptosis gauri privacy mitochondrial transmembrane potential bcl-2 family proteins wild type bcl-2 explore content subscription content inhibiting apoptosis induced apoptosis-related genes european economic area serum starvation/myc spatially distinct pathways issue learn institutional subscriptions read drs radhey gupta senior scientist award institut gustave roussy lysophosphatidic acid synthesis chronic liver disease accepting optional cookies journals search log manage preferences endoplasmic reticulum b-cell malignancies content late event matthew bcl-2 proteins https bcl-cb5 article purchase

Schema {🗺️}

WebPage:
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         headline:Endoplasmic reticulum localized Bcl-2 prevents apoptosis when redistribution of cytochrome c is a late event
         description:The disruption of mitochondrial function is a key component of apoptosis in most cell types. Localization of Bcl-2 to the outer mitochondrial and endoplasmic reticulum membranes is consistent with a role in the inhibition of many forms of apoptosis. In Rat-1 cells, a Bcl-2 mutant targeted exclusively to the endoplasmic reticulum (Bcl-cb5) was effective at inhibiting apoptosis induced by serum starvation/myc, or ceramide but not apoptosis induced by etoposide. The former conditions cause a decrease in mitochondrial transmembrane potential (Δψm) as an early event that precedes the release of cytochrome c from mitochondria. By contrast, when cells are exposed to etoposide, a situation in which cytochrome c release and membrane localization of the pro-apoptotic protein Bax precede loss of Δψm, wild type Bcl-2 but not Bcl-cb5 prevents apoptosis. Therefore, Bcl-2 functions in spatially distinct pathways of apoptosis distinguished by the order of cytochrome c release and loss of Δψm.
         datePublished:
         dateModified:
         pageStart:1939
         pageEnd:1952
         sameAs:https://doi.org/10.1038/sj.onc.1204288
         keywords:
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            Bax
            Bcl-2
            cytochrome c
            endoplasmic reticulum
            Medicine/Public Health
            general
            Internal Medicine
            Cell Biology
            Human Genetics
            Oncology
            Apoptosis
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      headline:Endoplasmic reticulum localized Bcl-2 prevents apoptosis when redistribution of cytochrome c is a late event
      description:The disruption of mitochondrial function is a key component of apoptosis in most cell types. Localization of Bcl-2 to the outer mitochondrial and endoplasmic reticulum membranes is consistent with a role in the inhibition of many forms of apoptosis. In Rat-1 cells, a Bcl-2 mutant targeted exclusively to the endoplasmic reticulum (Bcl-cb5) was effective at inhibiting apoptosis induced by serum starvation/myc, or ceramide but not apoptosis induced by etoposide. The former conditions cause a decrease in mitochondrial transmembrane potential (Δψm) as an early event that precedes the release of cytochrome c from mitochondria. By contrast, when cells are exposed to etoposide, a situation in which cytochrome c release and membrane localization of the pro-apoptotic protein Bax precede loss of Δψm, wild type Bcl-2 but not Bcl-cb5 prevents apoptosis. Therefore, Bcl-2 functions in spatially distinct pathways of apoptosis distinguished by the order of cytochrome c release and loss of Δψm.
      datePublished:
      dateModified:
      pageStart:1939
      pageEnd:1952
      sameAs:https://doi.org/10.1038/sj.onc.1204288
      keywords:
         apoptosis
         Bax
         Bcl-2
         cytochrome c
         endoplasmic reticulum
         Medicine/Public Health
         general
         Internal Medicine
         Cell Biology
         Human Genetics
         Oncology
         Apoptosis
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Social Networks {👍}(1)

External Links {🔗}(121)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.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
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