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  6. How Much Does Nature.com Make
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We are analyzing https://www.nature.com/articles/cr2012108.

Title:
LKB1-AMPK axis revisited | Cell Research
Description:
The LKB1 tumor suppressor encodes a serine-threonine kinase whose substrates control cell metabolism, polarity, and motility. LKB1 is a major mediator of the cellular response to energy stress via activation of the master regulator of energy homeostasis, AMPK. While mutational inactivation of LKB1 promotes the development of many types of epithelial cancer, a recent report in Nature by Jeon et al. demonstrates that the LKB1-AMPK pathway can also have an unexpected positive role in tumorigenesis, acting to maintain metabolic homeostasis and attenuate oxidative stress thereby supporting the survival of cancer cells.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {πŸ“š}

  • Science
  • Health & Fitness
  • Telecommunications

Content Management System {πŸ“}

What CMS is nature.com built with?

Custom-built

No common CMS systems were detected on Nature.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of nature.com 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.
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How Does Nature.com Make Money? {πŸ’Έ}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

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Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {πŸ’°}


Display Ads {🎯}

$63,100 per month
Our estimates place Nature.com's monthly online earnings from display ads at $42,042 to $115,616.

Keywords {πŸ”}

lkb, cell, cancer, cells, ampk, nature, pubmed, article, stress, tumor, lkbampk, survival, energy, acc, google, scholar, inactivation, cas, pathway, axis, metabolic, activation, nadph, central, function, research, kinase, role, mtor, authors, glucose, suppressor, control, metabolism, growth, fatty, cookies, content, bardeesy, response, epithelial, important, acid, privacy, polarity, homeostasis, types, jeon, mechanisms, processes,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy advertising acute nature social media amp-activated protein kinase 5β€²-amp-activated protein kinase nature nature 2002 nature 2012 nature 2007 author correspondence lkb1-ampk axis revisited development acetyl-coa carboxylase alpha acetyl-coa carboxylase beta lkb1-deficient lung cancer p53 dominant-negative coexpression glucose-starved a549 cells oxidized glutathione/reduced glutathione study lkb1-ampk-dependent survival lkb1-deficient tumors bypass lkb1-ampk-acc1/2-nadph pathway starvation-induced cell death context-specific tumor suppressor personal data lkb1-deficient cancer cells lkb1/stk11 inactivation leads article kottakis data protection tca-oxidative phosphorylation cycles permissions lkb1-mediated tumor suppression anchorage-independent conditions inhibited starvation-induced death increasing cellular amp serine-threonine kinase tumor suppressor emerges nabeel bardeesy rescue cell death shaw rj important ampk-independent functions established tumor suppressor enhanced cell survival cancer cell lines privacy improved cell survival lkb1 phosphorylates ampk energy stress-induced apoptosis

Questions {❓}

  • Based on these results, a major question is raised: How do LKB1-deficient tumors bypass the normal requirement for the LKB1-AMPK axis in energy stress response?

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:LKB1-AMPK axis revisited
         description:The LKB1 tumor suppressor encodes a serine-threonine kinase whose substrates control cell metabolism, polarity, and motility. LKB1 is a major mediator of the cellular response to energy stress via activation of the master regulator of energy homeostasis, AMPK. While mutational inactivation of LKB1 promotes the development of many types of epithelial cancer, a recent report in Nature by Jeon et al. demonstrates that the LKB1-AMPK pathway can also have an unexpected positive role in tumorigenesis, acting to maintain metabolic homeostasis and attenuate oxidative stress thereby supporting the survival of cancer cells.
         datePublished:2012-07-17T00:00:00Z
         dateModified:2012-07-17T00:00:00Z
         pageStart:1617
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         sameAs:https://doi.org/10.1038/cr.2012.108
         keywords:
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            Oncogenesis
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                        type:PostalAddress
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                     name:Massachusetts General Hospital Cancer Center, Harvard Medical School
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                        name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
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ScholarlyArticle:
      headline:LKB1-AMPK axis revisited
      description:The LKB1 tumor suppressor encodes a serine-threonine kinase whose substrates control cell metabolism, polarity, and motility. LKB1 is a major mediator of the cellular response to energy stress via activation of the master regulator of energy homeostasis, AMPK. While mutational inactivation of LKB1 promotes the development of many types of epithelial cancer, a recent report in Nature by Jeon et al. demonstrates that the LKB1-AMPK pathway can also have an unexpected positive role in tumorigenesis, acting to maintain metabolic homeostasis and attenuate oxidative stress thereby supporting the survival of cancer cells.
      datePublished:2012-07-17T00:00:00Z
      dateModified:2012-07-17T00:00:00Z
      pageStart:1617
      pageEnd:1620
      sameAs:https://doi.org/10.1038/cr.2012.108
      keywords:
         Cell signalling
         Oncogenesis
         Tumour suppressors
         Life Sciences
         general
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            name:Filippos Kottakis
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                  name:Massachusetts General Hospital Cancer Center, Harvard Medical School
                  address:
                     name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Nabeel Bardeesy
            affiliation:
                  name:Massachusetts General Hospital Cancer Center, Harvard Medical School
                  address:
                     name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
                     type:PostalAddress
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      name:Cell Research
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      name:Nature Publishing Group UK
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         type:ImageObject
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School
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         name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
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      name:Massachusetts General Hospital Cancer Center, Harvard Medical School
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         name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
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      name:Filippos Kottakis
      affiliation:
            name:Massachusetts General Hospital Cancer Center, Harvard Medical School
            address:
               name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      name:Nabeel Bardeesy
      affiliation:
            name:Massachusetts General Hospital Cancer Center, Harvard Medical School
            address:
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      name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA

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