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We are analyzing https://www.nature.com/articles/4401183.

Title:
Decision making by p53: life, death and cancer | Cell Death & Differentiation
Description:
The p53 tumor-suppressor plays a critical role in the prevention of human cancer. In the absence of cellular stress, the p53 protein is maintained at low steady-state levels and exerts very little, if any, effect on cell fate. However, in response to various types of stress, p53 becomes activated; this is reflected in elevated protein levels, as well as augmented biochemical capabilities. As a consequence of p53 activation, cells can undergo marked phenotypic changes, ranging from increased DNA repair to senescence and apoptosis. This review deals with the mechanisms that underlie the apoptotic activities of p53, as well as the complex interactions between p53 and central regulatory signaling networks. In p53-mediated apoptosis, the major role is played by the ability of p53 to transactivate specific target genes. The choice of particular subsets of target genes, dictated by covalent p53 modifications and protein–protein interactions, can make the difference between life and apoptotic death of a cell. In addition, transcriptional repression of antiapoptotic genes, as well as transcription-independent activities of p53, can also contribute to the apoptotic effects of p53. Regarding the crosstalk between p53 and signaling networks, this review focuses on the interplay between p53 and two pivotal regulatory proteins: β-catenin and Akt/PKB. Both proteins can regulate p53 as well as be regulated by it. In addition, p53 interacts with the GSK-3β kinase, which serves as a link between Akt and β-catenin. This review discusses how the functional balance between these different interactions might dictate the likelihood of a given cell to become cancerous or be eliminated from the replicative pool, resulting in suppression of cancer.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {📚}

  • Science
  • Telecommunications
  • Education

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Custom-built

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What is the average monthly size of nature.com audience?

🌆 Monumental Traffic: 20M - 50M visitors per month


Based on our best estimate, this website will receive around 42,799,894 visitors per month in the current month.

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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 {🎯}

$539,300 per month
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Keywords {🔍}

pubmed, google, scholar, cas, cell, apoptosis, genes, cancer, activation, central, βcatenin, protein, akt, target, apoptotic, mdm, transcriptional, cells, death, response, gene, figure, dna, biol, pmediated, activity, nature, mol, role, stress, growth, phosphorylation, conditions, degradation, human, ability, proteins, kinase, survival, function, tumorsuppressor, antiapoptotic, inactivation, binding, expression, additional, arrest, arf, oren, effects,

Topics {✒️}

nature portfolio permissions reprints privacy policy exact biochemical nature precise biochemical nature advertising tumor development cancer research intensive research high-risk human papillomaviruses research performed social media glycogen synthase kinase-3beta service author information authors nature nature 408 nature 404 nature 376 nature 416 nature 370 del sal emerging β-catenin-driven tumors author correspondence small-cell lung carcinoma deregulated beta-catenin induces rate-limiting transcription factor low steady-state levels n-terminal transcription domain blivet-van eggelpoel mj central tumor-suppressor n-terminal transactivation domain pi3k/akt signaling cascades wt1 tumor-suppressor protein β-catenin strongly induces nucleic acids res sequence-specific transcriptional activator breast cancer cells beta-catenin degradation linked putative tumor-suppressor zac-136 choroid plexus-derived tumors personal data squamous cell carcinomas transcription-coupled dna repair additional death-promoting genes uncoupling β-catenin deregulation pivotal tumor-suppressor gene received great attention transcription factor nf-κb glycogen synthase kinase-3

Questions {❓}

  • Beta catenin, Akt and p53: dancing together?
  • How do covalent modifications impact on the ability of p53 to choose among distinct transcriptional targets?
  • How does p53 inhibit or delay apoptosis?
  • Selective target gene activation: the sure road to the gallows?
  • So how does p53 trigger apoptosis when it is allowed to do so?
  • Transcriptional repression by p53: a role in apoptosis?
  • P53, Mdm2 and Akt: a matter of balance?

Schema {🗺️}

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