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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).

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Science
Health & Fitness
Telecommunications

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Custom-built

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

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How Much Does Nature.com Make? {💰}

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$63,100 per month
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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:
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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
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      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.
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