AMP-Activated Protein Kinase and Autophagy

Meijer, Alfred J.; Codogno, Patrice

doi:10.4161/auto.3710

Cited by 151 publications

(112 citation statements)

References 28 publications

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“…The decrease in mTOR phosphorylation was particularly pronounced for Ser 2448 , a phosphorylation event that occurs in the presence of amino acids by upstream signaling factors including AKT. 32,33,36 The decrease in the levels of autophosphorylated form of mTOR, at Ser 2481 , was more pronounced in the chronically inhibited Fig. 5A and B), although whether or not these differences contribute to the different rates of macroautophagy observed in these cells is yet unclear, it is possible that alterations in AMPK signaling following CMA blockage contribute to the described changes in macroautophagy in these cells.…”

Section: Changes In Macroautophagy Upon Acute Cma Blockagementioning

confidence: 88%

“…We compared total levels of mTOR and of the 24 AMPK has therefore been proposed to play a critical role in modulation of macroautophagy. [32][33][34][35][36] The third phosphorylation site, an auto-phosphorylation at Ser 2481 , has been described under translationally repressive conditions, 25 thereby possibly also playing a role in regulation of macroautophagy. We found slightly lower levels of mTOR in acutely CMA inhibited cells, which persist and decrease even more in the chronically inhibited cells when compared with control cells (Fig.…”

Section: Changes In Macroautophagy Upon Acute Cma Blockagementioning

confidence: 99%

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Early cellular changes after blockage of chaperone-mediated autophagy

et al. 2008

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Cytosolic proteins can be selectively degraded in lysosomes by chaperone-mediated autophagy (CMA), an autophagic pathway maximally activated under stress. In previous works we have demonstrated the existence of a cross-talk between CMA and macroautophagy, the other stress-related autophagic pathway responsible for the "in bulk" degradation of whole regions of the cytosol and for organelle turnover. We found that chronic blockage of CMA, as the one described in aging cells, results in constitutive activation of macroautophagy, supporting that one pathway may compensate for the other. In this work we have investigated the series of early cellular events that precede the activation of macroautophagy upon CMA blockage and the consequences of this blockage on cellular homeostasis. Shortly after CMA blockage, we have found functional alterations in macroautophagy and the ubiquitin-proteasome system, that are progressively corrected as CMA blockage persists. Basal macroautophagic activity remains initially unaltered, but we observed a delay in its activation in response to serum removal, a well characterized inducer for this pathway. Slower degradation of short-lived proteins, and a transient decrease in some of the proteasome proteolytic activities are also evident in the first stages of CMA blockage. This global alteration of the proteolytic systems supports the coordinated functioning of all of them, and seems responsible for the intracellular accumulation of altered proteins. Based on the time-course of the cellular changes, we propose that a minimal threshold of these toxic products needs to accumulate in order to constitutively activate macroautophagy and thus return cellular homeostasis to normal.

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Section: Changes In Macroautophagy Upon Acute Cma Blockagementioning

confidence: 88%

Section: Changes In Macroautophagy Upon Acute Cma Blockagementioning

confidence: 99%

Early cellular changes after blockage of chaperone-mediated autophagy

et al. 2008

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“…1E). In addition, it is well recognized that AMPK activation promotes autophagy in cancer cells via mTOR inhibition (27). The ability of OSU-53 to induce autophagy concomitantly with apoptosis was manifested by the parallel conversion of LC3-I to LC3-II in MDA-MB-231 cells (Fig.…”

Section: Osu-53 a Direct Activator Of Ampk Exhibits High Potency Inmentioning

confidence: 99%

Targeting Energy Metabolic and Oncogenic Signaling Pathways in Triple-negative Breast Cancer by a Novel Adenosine Monophosphate-activated Protein Kinase (AMPK) Activator

Lee

Hsu

Guh

et al. 2011

Journal of Biological Chemistry

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Background: Adenosine monophosphate-activated protein kinase (AMPK) modulates cancer cell metabolism and survival. Results: The novel compound OSU-53 directly activates AMPK, inhibits multiple metabolic and oncogenic pathways, and induces apoptosis in triple-negative breast cancer cells. Conclusion: OSU-53 acts through a broad spectrum of antitumor activities downstream of AMPK activation. Significance: OSU-53 is a potent small molecule AMPK activator with translational potential for breast cancer therapy.

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“…The activation of AMPK due to the activated tumor suppressor, p53, leads to inhibition of the mTOR activity and subsequent induction of autophagy (40). It has been reported that the activity of AMPK is essential for the process and regulation of autophagy (41,42). In addition Hansen and Jaattela (43) proposed that increased levels of free cytosolic Ca…”

Section: Regulation Of Autophagymentioning

confidence: 99%

Autophagy-Is it a preferred route for lifespan extension?

Dwivedi

Ahnn

2009

BMB Reports

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Autophagy, which is a process of self eating, has gained interest in the past decade due to its both beneficial and controversial roles in various biological phenomena. The discovery of autophagy genes (ATG) in yeast has led to focused research designed to elucidate the mechanism and regulation of this process. The role of autophagy in a variety of biological phenomena, including human disease, is still the subject of debate. However, recent findings suggest that autophagy is a highly regulated process with both beneficial and negative effects. Indeed, studies conducted using various model organisms have demonstrated that increased autophagy leads to an extended lifespan. Despite these findings, it is still unknown if all pathways leading to extended lifespan converge at the process of autophagy or not. Here, an overview of modern developments related to the process of autophagy, its regulation and the molecular machinery involved is presented. In addition, this review focuses on one of the beneficial aspects of autophagy, its role in lifespan regulation. [BMB reports 2009; 42(2): 65-71]

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AMP-Activated Protein Kinase and Autophagy

Cited by 151 publications

References 28 publications

Early cellular changes after blockage of chaperone-mediated autophagy

Early cellular changes after blockage of chaperone-mediated autophagy

Targeting Energy Metabolic and Oncogenic Signaling Pathways in Triple-negative Breast Cancer by a Novel Adenosine Monophosphate-activated Protein Kinase (AMPK) Activator

Autophagy-Is it a preferred route for lifespan extension?

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