
Cell Metabolism, Год журнала: 2012, Номер 16(4), С. 414 - 419
Опубликована: Сен. 20, 2012
Язык: Английский
Cell Metabolism, Год журнала: 2012, Номер 16(4), С. 414 - 419
Опубликована: Сен. 20, 2012
Язык: Английский
Nature Reviews Molecular Cell Biology, Год журнала: 2012, Номер 13(4), С. 239 - 250
Опубликована: Март 22, 2012
Язык: Английский
Процитировано
1083Science, Год журнала: 2016, Номер 351(6270), С. 275 - 281
Опубликована: Янв. 15, 2016
Mitochondria undergo fragmentation in response to electron transport chain (ETC) poisons and mitochondrial DNA-linked disease mutations, yet how these stimuli mechanistically connect the fission fusion machinery is poorly understood. We found that energy-sensing adenosine monophosphate (AMP)-activated protein kinase (AMPK) genetically required for cells rapid after treatment with ETC inhibitors. Moreover, direct pharmacological activation of AMPK was sufficient rapidly promote even absence stress. A screen substrates identified factor (MFF), a outer-membrane receptor DRP1, cytoplasmic guanosine triphosphatase catalyzes fission. Nonphosphorylatable phosphomimetic alleles sites MFF revealed it key effector AMPK-mediated
Язык: Английский
Процитировано
947Experimental & Molecular Medicine, Год журнала: 2016, Номер 48(7), С. e245 - e245
Опубликована: Июль 15, 2016
5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine that was originally identified as the key player in maintaining cellular energy homeostasis. Intensive research over last decade has diverse molecular mechanisms and physiological conditions regulate AMPK activity. regulates metabolic processes dysregulated major chronic diseases, such obesity, inflammation, diabetes cancer. On basis of its critical roles physiology pathology, emerging one most promising targets for both prevention treatment these diseases. In this review, we discuss current understanding regulation functions. addition, underlying versatile Therapies based on enzyme involved balance may help prevent treat cancer, obesity diabetes. Sang-Min Jeon at Ajou University Suwon, South Korea, reviewed ‘5’-AMP-activated kinase' (AMPK), potential to Among other tasks, maintains cells by regulating glucose levels oxidizing fatty acids. Research indicates are suppressed over-eating, triggering insulin resistance hence Reducing can also induce a component diseases like Jeon's review finds evidence activating patients could progression A similar technique fight early-stage carcinogenesis. However, warns exacerbate later-stage carcinogenesis established cancer tumors.
Язык: Английский
Процитировано
944Nature Reviews Endocrinology, Год журнала: 2017, Номер 13(12), С. 710 - 730
Опубликована: Авг. 29, 2017
Язык: Английский
Процитировано
912Cell Metabolism, Год журнала: 2012, Номер 17(1), С. 113 - 124
Опубликована: Дек. 27, 2012
AMPK is a metabolic sensor that helps maintain cellular energy homeostasis. Despite evidence linking with tumor suppressor functions, the role of in tumorigenesis and metabolism unknown. Here we show negatively regulates aerobic glycolysis (the Warburg effect) cancer cells suppresses growth vivo. Genetic ablation α1 catalytic subunit accelerates Myc-induced lymphomagenesis. Inactivation AMPKα both transformed nontransformed promotes shift to glycolysis, increased allocation glucose carbon into lipids, biomass accumulation. These effects require normoxic stabilization hypoxia-inducible factor-1α (HIF-1α), as silencing HIF-1α reverses biosynthetic proliferative advantages conferred by reduced signaling. Together our findings suggest activity opposes development its loss fosters progression part regulating pathways support cell proliferation.
Язык: Английский
Процитировано
837Nature Medicine, Год журнала: 2013, Номер 19(12), С. 1649 - 1654
Опубликована: Ноя. 3, 2013
Язык: Английский
Процитировано
790Disease Models & Mechanisms, Год журнала: 2013, Номер 6(6), С. 1353 - 1363
Опубликована: Ноя. 1, 2013
An increased rate of lipid synthesis in cancerous tissues has long been recognised as an important aspect the rewired metabolism transformed cells. However, contribution lipids to cellular transformation, tumour development and progression, well their potential role facilitating spread cells secondary sites, are not yet fully understood. In this article, we review recent findings that support importance tumorigenesis. Specifically, explore aberrant biosynthesis cancer cell migration invasion, induction angiogenesis. These processes crucial for dissemination formation metastases, which constitute main cause mortality.
Язык: Английский
Процитировано
706The Journal of Experimental Medicine, Год журнала: 2020, Номер 218(1)
Опубликована: Дек. 18, 2020
Dysregulation in lipid metabolism is among the most prominent metabolic alterations cancer. Cancer cells harness to obtain energy, components for biological membranes, and signaling molecules needed proliferation, survival, invasion, metastasis, response tumor microenvironment impact cancer therapy. Here, we summarize discuss current knowledge about advances made understanding regulation of introduce different approaches that have been clinically used disrupt
Язык: Английский
Процитировано
652Experimental & Molecular Medicine, Год журнала: 2016, Номер 48(3), С. e218 - e218
Опубликована: Март 11, 2016
Glucose homeostasis is tightly regulated to meet the energy requirements of vital organs and maintain an individual's health. The liver has a major role in control glucose by controlling various pathways metabolism, including glycogenesis, glycogenolysis, glycolysis gluconeogenesis. Both acute chronic regulation enzymes involved are required for proper functioning these complex interwoven systems. Allosteric metabolic intermediates, as well post-translational modifications constitute pathways, controlled expression genes encoding critical mediating longer-term pathways. Notably, several key transcription factors shown be metabolism gluconeogenesis liver. In this review, we would like illustrate current understanding with emphasis on their regulators that homeostasis. Hundreds body's processing glucose. Together help body blood levels convert excessive carbohydrates into fatty acids. Seung-Hoi Koo colleagues at Korea University. researchers explain how different factors, sterol regulatory element binding protein 1c (SREBP-1c), carbohydrate response (ChREBP), cAMP element-binding (CREB) forkhead box O1 (FoxO1). Specifically, SREBP-1c ChREBP responsible activation acid biosynthesis, while CREB FoxO1 gluconeogenesis—the production from non-carbohydrate sources.
Язык: Английский
Процитировано
641Cell Metabolism, Год журнала: 2011, Номер 14(1), С. 21 - 32
Опубликована: Июль 1, 2011
Язык: Английский
Процитировано
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