Akt maintains cell size and survival by increasing mTOR-dependent nutrient uptake.

By A. Edinger, Craig B. Thompson. Molecular Biology of the Cell, 2002

617 citations recorded by the source corpus.

Subfields: Biochemistry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/30a06dffb72f7b88a22beeeeebb84fe51fa47eb4

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Citations in the corpus

TOR signaling in growth and metabolism. (2006, background): “Similarly, mTORC1 controls trafficking of nutrient transporters and thereby promotes uptake of nutrients such as glucose, amino acids, lipoprotein, and iron (Edinger and Thompson, 2002).”
Akt-Directed Glucose Metabolism Can Prevent Bax Conformation Change and Promote Growth Factor-Independent Survival (2003, background): “The latter hypothesis is supported by observations with both hematopoietic and neuronal systems that cellular metabolism normally decreases upon withdrawal from growth factor (12, 49, 61) but that Akt can prevent this decline (15, 48) and that Akt can promote short-term survival even in the presence”
TOR signalling in bugs, brain and brawn (2003, background): “Interestingly, mTOR also inhibits autophagy and nutrient transporter turnover in mammalian cells, but the mechanism of this inhibition is unknow”
Glucose Uptake Is Limiting in T Cell Activation and Requires CD28-Mediated Akt-Dependent and Independent Pathways1 (2008, background): “in lysosomes to restrict glucose uptake (17, 19).”
Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “While enforced high expression of BCL-xL can provide long-term protection from apoptosis, AKT does not seem to provide as much long-term protection (Edinger and Thompson, 2002; Plas et al., 2001).”
Role and regulation of starvation-induced autophagy in the Drosophila fat body. (2004, background): “Alternational functions in cells with depressed TOR signaling, tively, as TOR activity is required for proper expression including recycling of organelles damaged by the aband localization of a number of nutrient transporters sence of TOR activity, or selective degradation of cell (Bogan et al., 200”
The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. (2008, background): “First, it permits cells to increase the surface expression of nutrient transporters, enabling increased uptake of glucose, amino acids, and other nutrients (Barata et al., 2004; Edinger and Thompson, 2002; Roos et al., 2007; Wieman et al., 2007; Xu et al., 2005).”
mTOR, translation initiation and cancer (2006, background): “…2004). eIF4E also blocks endoplasmic reticulum- and p53-mediated apoptosis (Li et al., 2004; Mungamuri et al., 2006). mTOR controls cell survival (Edinger and Thompson, 2002; Mungamuri et al., 2006). eIF4E could serve as an important downstream effector of mTOR in the control of cell survival…”
Akt Stimulates Aerobic Glycolysis in Cancer Cells (2004, background): “regulate transporters for both amino acids and lipids (39).”
PI3 Kinase signals BCR dependent mature B cell survival (2009, neutral): “Additional candidate PI3K targets include the regulators of cell size and metabolism, mTOR (Edinger and Thompson, 2002), in line with the failure of FOXO1 deletion to rescue BCR cell size.”
mTOR inhibition reverses Akt-dependent prostate intraepithelial neoplasia through regulation of apoptotic and HIF-1-dependent pathways (2004, result): “These latter data are in keeping with the observation that rapamycin decreases the mitochondrial membrane potential of cells expressing activated AK”
Bidirectional Transport of Amino Acids Regulates mTOR and Autophagy (2009, positive): “described previously ( Edinger and Thompson, 2002 ) with specific details described in the supplementary information.”