An emerging role of mTOR in lipid biosynthesis
By M. Laplante, David M. Sabatini. Current Biology, 2009
641 citations recorded by the source corpus.
Lipid biosynthesis is essential for the maintenance of cellular homeostasis. The lipids produced by cells (glycerolipids, fatty acids, phospholipids, cholesterol, spingolipids) are used as an energy source/reserve, as building blocks for membrane biosynthesis, as precursor molecules for the synthesis of various cellular products and as signaling molecules. Defects in lipid synthesis or processing contribute to the development of many diseases, including obesity, insulin resistance, type 2 diabetes, non-alcoholic fatty liver disease, and cancer. Studies published over the last few years have shown that the target of rapamycin (TOR), a conserved serine/threonine kinase playing key roles in regulating cell growth, controls lipid biosynthesis through various mechanisms. Here, we review these findings and briefly discuss their potential relevance for human health and disease.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/3d33ad2b456ea578e2290f54b4318f0c0c02ae62
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Citations in the corpus
- Mitochondrial complex III ROS regulate adipocyte differentiation (2011, positive): “…Is Required for the Early Increase in ROS during Adipocyte Differentiation PI3-kinase signaling pathway and its downstream effector mTORC1 are well-characterized regulators of lipogenesis and PPARg-dependent transcription during adipocyte differentiation (Laplante and Sabatini, 2009).”
- The Lin28/let-7 axis regulates glucose metabolism (2011, background): “Reprogramming toward glyco- lytic metabolism can increase a cancer cell’s ability to generate biomass, a phenomenon termed the ‘‘Warburg Effect’’ (Denko, 2008; Engelman et al., 2006; Gao et al., 2009; Guertin and Sabatini, 2007; Laplante and Sabatini, 2009; Vander Heiden et al., 2009; Yun et al., 20”
- Cellular Fatty Acid Metabolism and Cancer (2013, background): “Further upstream, SREBP transcription factors and FA synthesis can be regulated by many signaling pathways, including growth factor signaling, which is reviewed in depth elsewhere (Shao and Espenshade, 2012; Kumar-Sinha et al., 2003; Peterson et al., 2011; Laplante and Sabatini, 2009; Lewis et al., ”
- Bifurcation of insulin signaling pathway in rat liver: mTORC1 required for stimulation of lipogenesis, but not inhibition of gluconeogenesis (2010, background): “ActivatedAkt phosphorylates Tuberous Sclerosis Complex 2 (TSC2), thereby initiating a chain of events that inactivates inhibitors of mTORC1 complex, leading to activation of themTOR kinase (20).”