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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
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  6. Keywords
  7. Topics
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We began analyzing https://www.nature.com/articles/ng0897-358, but it redirected us to https://www.nature.com/articles/ng0897-358. The analysis below is for the second page.

Title[redir]:
Bcl-2 and Bax function independently to regulate cell death | Nature Genetics
Description:
The BCL-2 family has various pairs of antagonist and agonist proteins that regulate apoptosis. Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2–deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between fiaxand Bax and Bcl-2, each is able to regulate apoptosis independently.

Matching Content Categories {📚}

  • Education
  • Telecommunications
  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

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

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


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How Does Doi.org Make Money? {💸}

The income method remains a mystery to us.

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Keywords {🔍}

article, google, scholar, cas, cell, bcl, nature, death, apoptosis, korsmeyer, bax, access, mice, family, protein, usa, content, proc, atal, acad, sci, cookies, bclxl, privacy, function, pubmed, data, journal, regulate, knudson, proteins, cancer, open, development, science, survival, dev, activation, protease, advertising, information, subscribe, genetics, independently, institution, buy, human, chromosome, promotes, cells,

Topics {✒️}

nature portfolio permissions reprints privacy policy advertising social media nature 335 nature 369 nature 379 nature 356 nature 381 nature 348 nature amyloid beta1–42-induced apoptosis b-cell neoplasms result personal data bax-induced cell death data protection permissions springerlink instant access promotes thymocyte differentiation murine development bcl-xl function upstream fas-induced activation cell death pathway—bcl-2 mitochondrial membrane protein development privacy immature hematopoietic cells ice protease cascade promotes cell death bcl-2 protein family bcl-2 family proteins programmed cell death protein binding functions explore content subscription content michael knudson & stanley european economic area thymic hypoplasia characteristic institutional subscriptions read transcriptionally active locus distorted small intestine trophic factor deprivation cd4+cd8+ stage washington university school chicken manure amendment statistical experimental designs colon cancer gaber defined neuroprotective agent bcl-2 protein expression

Schema {🗺️}

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      headline:Bcl-2 and Bax function independently to regulate cell death
      description:The BCL-2 family has various pairs of antagonist and agonist proteins that regulate apoptosis. Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2–deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between fiaxand Bax and Bcl-2, each is able to regulate apoptosis independently.
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External Links {🔗}(187)

Analytics and Tracking {📊}

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Libraries {📚}

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CDN Services {📦}

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