Expanding Roles for SREBP in Metabolism DOI Creative Commons
Wei Shao, Peter J. Espenshade

Cell Metabolism, Journal Year: 2012, Volume and Issue: 16(4), P. 414 - 419

Published: Sept. 20, 2012

Language: Английский

MicroRNAs in metabolism and metabolic disorders DOI

Veerle Rottiers,

Anders M. Näär

Nature Reviews Molecular Cell Biology, Journal Year: 2012, Volume and Issue: 13(4), P. 239 - 250

Published: March 22, 2012

Language: Английский

Citations

1082

AMP-activated protein kinase mediates mitochondrial fission in response to energy stress DOI
Erin Quan Toyama, Sébastien Herzig, Julien Courchet

et al.

Science, Journal Year: 2016, Volume and Issue: 351(6270), P. 275 - 281

Published: Jan. 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

Language: Английский

Citations

937

Regulation and function of AMPK in physiology and diseases DOI Creative Commons
Sang‐Min Jeon

Experimental & Molecular Medicine, Journal Year: 2016, Volume and Issue: 48(7), P. e245 - e245

Published: July 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.

Language: Английский

Citations

933

SREBP-regulated lipid metabolism: convergent physiology — divergent pathophysiology DOI
Hitoshi Shimano, Ryuichiro Sato

Nature Reviews Endocrinology, Journal Year: 2017, Volume and Issue: 13(12), P. 710 - 730

Published: Aug. 29, 2017

Language: Английский

Citations

904

AMPK Is a Negative Regulator of the Warburg Effect and Suppresses Tumor Growth In Vivo DOI Creative Commons
Brandon Faubert,

Gino Boily,

Said Izreig

et al.

Cell Metabolism, Journal Year: 2012, Volume and Issue: 17(1), P. 113 - 124

Published: Dec. 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.

Language: Английский

Citations

835

Single phosphorylation sites in Acc1 and Acc2 regulate lipid homeostasis and the insulin-sensitizing effects of metformin DOI
Morgan D. Fullerton, Sandra Galić,

Katarina Marcinko

et al.

Nature Medicine, Journal Year: 2013, Volume and Issue: 19(12), P. 1649 - 1654

Published: Nov. 3, 2013

Language: Английский

Citations

785

Hooked on fat: the role of lipid synthesis in cancer metabolism and tumour development DOI Creative Commons
Franziska Baenke, Barrie Peck,

Heike Miess

et al.

Disease Models & Mechanisms, Journal Year: 2013, Volume and Issue: 6(6), P. 1353 - 1363

Published: Nov. 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.

Language: Английский

Citations

705

Regulation of glucose metabolism from a liver-centric perspective DOI Creative Commons

Hye-Sook Han,

Geon Kang,

Jun Seok Kim

et al.

Experimental & Molecular Medicine, Journal Year: 2016, Volume and Issue: 48(3), P. e218 - e218

Published: March 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.

Language: Английский

Citations

636

Lipid metabolism and cancer DOI Creative Commons
Xueli Bian, Rui Liu, Ying Meng

et al.

The Journal of Experimental Medicine, Journal Year: 2020, Volume and Issue: 218(1)

Published: Dec. 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

Language: Английский

Citations

623

Akt Stimulates Hepatic SREBP1c and Lipogenesis through Parallel mTORC1-Dependent and Independent Pathways DOI Creative Commons

Jessica L. Yecies,

Huihui Zhang,

Suchithra Menon

et al.

Cell Metabolism, Journal Year: 2011, Volume and Issue: 14(1), P. 21 - 32

Published: July 1, 2011

Language: Английский

Citations

580