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We began analyzing https://www.tandfonline.com/doi/abs/10.4161/cbt.26726, but it redirected us to https://www.tandfonline.com/doi/abs/10.4161/cbt.26726. The analysis below is for the second page.

Title[redir]:
Full article: AMP-activated protein kinase (AMPK) beyond metabolism
Description:
The ability of living organisms to maintain normal function and longevity is intricately linked with their ability to adapt to the physiological challenges that arise in a continuously changing env...

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Keywords {🔍}

open, window, ampk, citation, cell, cells, cancer, google, scholar, pubmed, pmid, science, web, atm, protein, radiation, kinase, phosphorylation, stress, ionizing, activation, cycle, activity, response, dna, expression, mitotic, cellular, mtor, inhibition, ampactivated, regulation, role, autophagy, damage, progression, survival, signaling, pathway, metabolic, energy, tumor, metabolism, biol, mitosis, ser, growth, pathways, ampkα, lung,

Topics {✒️}

amp mimetic 5-aminoimidazole-4-carboxamide-1-b-4-ribofuranoside 3-hydroxy-3-methyl-glutaryl-coa reductase diet-induced insulin-resistant mice dna double-strand breaks calmodulin-dependent protein kinase serine79-phosphorylated acetyl-coa carboxylase amp-activated protein kinase p21-activated protein kinase amp-activated kinase alpha akt-mtor pro-survival pathway cyclin-dependent kinase inhibitor nad-dependent protein deacetylase dna-dependent protein kinase atm-mediated lkb1-thr366 phosphorylation forming intra-strand crosslinks sánchez-arévalo lobo vj induce spindle mis-orientation google scholar moreno-sánchez google scholar fernandez-capetillo small g-protein rheb serine/threonine protein kinase google scholar vazquez-martin phospho-ser10-h3 signal akt-mtor-p70s6k/4-ebp1 pathway igf-1-akt-mtor pathways google scholar bettencourt-dias review data p53-dependent transcriptional upregulation ionizing radiation-induced apoptosis p53-null cancer cells lkb1/ampk/tsc/mtorc1 signaling induce atm-dependent activation cisplatin-induced dna damage twitter page taylor radiation-induced atm activity ionizing radiation-induced g2/ g2-cell cycle arrest global anti-tumor action akt-mtor signaling cascade bak-induced apoptosis google scholar linher-melville mouse embryonic fibroblasts article introduction ampk 5-aminoimidazole-4-carboxamide ribonucleoside francis group genomic stress-mediated activation mediates dna breaks alter mitotic progression metformin-mediated metabolic stress rad3-related protein

Questions {❓}

A specific method for activating AMP-activated protein kinase in intact cells?
AMP-activated protein kinase: also regulated by ADP?
The above findings impose a key underlying question: What is the mechanism by which radiotherapy enhances chronically ATM-AMPK-p53 pathway expression and inhibits Akt/mTOR?

Schema {🗺️}

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      articleSection:Review
      name:AMP-activated protein kinase (AMPK) beyond metabolism
      headline:AMP-activated protein kinase (AMPK) beyond metabolism
      abstract:AMP-activated protein kinase (AMPK), an established metabolic stress sensor, has gained popularity in cancer biology due to its ability to control cellular growth and mediate cell cycle checkpoints in cancer cells in response to low energy levels. AMPK is a key effector of the tumor suppressor liver kinase B 1 (LKB1) which inhibits the cellular growth mediator mammalian target of rapamycin (mTOR) and activates checkpoint mediators such as p53 and the cyclin dependent kinase inhibitors p21cip1 and p27kip1. However, recent work describes a novel function for AMPK as a sensor of genomic stress and a participant of the DNA damage response (DDR) pathway. Ionizing radiation and chemotherapy activate AMPK in cancer cells to mediate signal transduction downstream of ataxia telangiectasia mutated (ATM) to activate p53- p21cip1/p27kip1 and inhibit mTOR. We discuss evidence on the transcriptional and post-translational regulation of AMPK by ionizing radiation and the role of the enzyme as a mediator of chemo- and radiation sensitivity in epithelial cancer cells. Furthermore, we review data on the participation of AMPK in cytokinesis and observations suggesting a physical association of this enzyme with the mitotic apparatus. The evidence available to date suggests that AMPK is a point of convergence of metabolic and genomic stress signals, which (1) control the activity of growth mediators, (2) propagate DDR, and (3) mediate the anti-proliferative effects of common cytotoxic cancer therapy such as radiation and chemotherapy. This highlights the importance of targeting AMPK with novel cancer therapeutics.
      description:AMP-activated protein kinase (AMPK), an established metabolic stress sensor, has gained popularity in cancer biology due to its ability to control cellular growth and mediate cell cycle checkpoints in cancer cells in response to low energy levels. AMPK is a key effector of the tumor suppressor liver kinase B 1 (LKB1) which inhibits the cellular growth mediator mammalian target of rapamycin (mTOR) and activates checkpoint mediators such as p53 and the cyclin dependent kinase inhibitors p21cip1 and p27kip1. However, recent work describes a novel function for AMPK as a sensor of genomic stress and a participant of the DNA damage response (DDR) pathway. Ionizing radiation and chemotherapy activate AMPK in cancer cells to mediate signal transduction downstream of ataxia telangiectasia mutated (ATM) to activate p53- p21cip1/p27kip1 and inhibit mTOR. We discuss evidence on the transcriptional and post-translational regulation of AMPK by ionizing radiation and the role of the enzyme as a mediator of chemo- and radiation sensitivity in epithelial cancer cells. Furthermore, we review data on the participation of AMPK in cytokinesis and observations suggesting a physical association of this enzyme with the mitotic apparatus. The evidence available to date suggests that AMPK is a point of convergence of metabolic and genomic stress signals, which (1) control the activity of growth mediators, (2) propagate DDR, and (3) mediate the anti-proliferative effects of common cytotoxic cancer therapy such as radiation and chemotherapy. This highlights the importance of targeting AMPK with novel cancer therapeutics.
      author:
            type:Person
            name:Gurmit Singh
            type:Person
            name:Toran Sanli
            type:Person
            name:Theodoros Tsakiridis
            type:Person
            name:Gregory R Steinberg
            type:Person
            name:Theodoros Tsakiridis
      keywords:AMPK, ionizing radiation, cell cycle, ATM, mitosis
      pageStart:156
      pageEnd:169
      datePublished:2013-11-01
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      name:Toran Sanli
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      name:Gregory R Steinberg
      name:Theodoros Tsakiridis
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