mTOR signaling in growth control and disease

By M. Laplante, David M. Sabatini. Cell, 2012

8,358 citations recorded by the source corpus.

The mammalian target of rapamycin (mTOR) signaling pathway senses and integrates a variety of environmental cues to regulate organismal growth and homeostasis. The pathway regulates many major cellular processes and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration. Here, we review recent advances in our understanding of the mTOR pathway and its role in health and disease as well as aging. We further discuss pharmacological approaches to treat human pathologies linked to mTOR deregulation.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9318ecf2867c03b77fa1ace9865cffa5ee6b9a30

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In Molecular Biology

Citations in the corpus

Fundamentals of cancer metabolism (2016, background): “mTORC1 is stimulated by the presence of amino acids and activates protein synthesis via its effects on translation and ribosome biogenesis (80).”
The PI3K/AKT pathway in obesity and type 2 diabetes (2018, background): “AKT-mediated mTORC1 activation regulates a number of downstream effectors proteins through phosphorylation, including the well-characterized effectors p70 ribosomal S6 protein kinase-1 (S6K1) and eukaryotic translation initiation factor-4E (eIF4E)binding protein-1 (4E-BP1), to increase protein synth”
MYC, Metabolism, and Cancer. (2015, background): “Lack of amino acids attenuates mTOR activity through sensing by the RAG proteins on the lysosomal membrane (84), thereby both diminishing protein synthesis and cellular processes that would consume nutrients and ATP and relieving the inhibitory block on autophagy (84).”
Glucose Metabolism Regulates T Cell Activation, Differentiation, and Functions (2014, background): “mTOR activation regulates a myriad of cellular functions, including growth, apoptosis, differentiation, and metabolism (31, 32).”
Phosphoinositides: tiny lipids with giant impact on cell regulation. (2013, background): “mTORC1 collects information through various pathways on cellular stress, energy levels, amino acids, and growth factors and controls cell growth, metabolism, cell cycle progression, and macroautophagy (854).”
The cell biology of disease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction. (2012, positive): “Central to this pathway is mTOR, a serine/threonine kinase that has an overarching role in coordinating cellular metabolism with nutritional status (Laplante and Sabatini, 2012).”
Autophagy and Neurodegeneration: Pathogenic Mechanisms and Therapeutic Opportunities. (2017, positive): “…to the ULK1 complex (via Raptor-ULK1 interaction), and by phosphorylating both ATG13 and ULK1 (at Ser 757), thereby suppressing ULK1 kinase activity and preventing the interaction between ULK1 and AMPK (Ganley et al., 2009; Hosokawa et al., 2009; Jung et al., 2009; Laplante and Sabatini, 2012).”
Autophagy in malignant transformation and cancer progression (2015, positive): “Besides inhibiting the catalytic activity of MTORCI, AMPK directly stimulates autophagy by phosphorylating ULK1 as well as phosphatidylinositol 3-kinase, catalytic subunit type 3 (PIK3C3, best known as VPS34) and Beclin 1 (BECN1, the mammalian ortholog of yeast Atg6), two components of a multiprotei”