NATURE . COM {}

Analyzed Page
Matching Content Categories
CMS
Monthly Traffic Estimate
How Does Nature.com Make Money
How Much Does Nature.com Make
Keywords
Topics
Questions
Schema
External Links
Analytics And Tracking
Libraries
Hosting Providers
CDN Services

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 {📚}

Science
Health & Fitness
Telecommunications

Content Management System {📝}

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 {📈}

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.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Nature.com Make Money? {💸}

Display Ads {🎯}

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

Ads are managed by yourbow.com. Particular relationships are as follows:

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? {💰}

Display Ads {🎯}

$63,100 per month
According to our algorithms, Nature.com's monthly online income from display advertising ranges from $42,042 to $115,616.

Keywords {🔍}

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 {✒️}

nature portfolio permissions reprints privacy policy advertising acute nature social media amp-activated protein kinase 5′-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 {🗺️}

WebPage:
      mainEntity:
         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
            Cell Biology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcr.2012.108/MediaObjects/41422_2012_Article_BFcr2012108_Fig1_HTML.jpg
         isPartOf:
            name:Cell Research
            issn:
               1748-7838
               1001-0602
            volumeNumber:22
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Nature Publishing Group UK
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               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
               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
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
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
         Cell Biology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1038%2Fcr.2012.108/MediaObjects/41422_2012_Article_BFcr2012108_Fig1_HTML.jpg
      isPartOf:
         name:Cell Research
         issn:
            1748-7838
            1001-0602
         volumeNumber:22
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Nature Publishing Group UK
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            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
            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
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Cell Research
      issn:
         1748-7838
         1001-0602
      volumeNumber:22
Organization:
      name:Nature Publishing Group UK
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School
      address:
         name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
         type:PostalAddress
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School
      address:
         name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      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:
               name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA
      name:Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, USA

External Links {🔗}(66)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Prism.js
Zoom.js

Emails and Hosting {✉️}

Mail Servers:

mxa-002c5801.gslb.pphosted.com
mxb-002c5801.gslb.pphosted.com

Name Servers:

pdns1.ultradns.net
pdns2.ultradns.net
pdns3.ultradns.org
pdns4.ultradns.org
pdns5.ultradns.info
pdns6.ultradns.co.uk

CDN Services {📦}

Crossref

4.57s.