Akt-Directed Glucose Metabolism Can Prevent Bax Conformation Change and Promote Growth Factor-Independent Survival

By J. Rathmell, C. Fox, D. Plas, P. Hammerman, Ryan M. Cinalli, Craig B. Thompson. Molecular and Cellular Biology, 2003

599 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/034588e38edf88b6f545e7ac502421e05a5f6b3b

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Citations in the corpus

Necrotic death as a cell fate. (2006, background): “In cultured cells, nutrient deprivation or growth factors withdrawal leads to apoptotic cell death initiated by proapoptotic Bcl-2 proteins (Lindsten et al. 2000; Rathmell et al. 2000, 2003; Wei et al. 2001).”
TRB3, a novel ER stress‐inducible gene, is induced via ATF4–CHOP pathway and is involved in cell death (2005, background): “In addition, it has been described that the dephosphorylation of Akt is essential to the Bax conformational change and translocation to mitochondria of Bax (Pervin et al, 2003; Rathmell et al, 2003).”
Hypoxia-Inducible Factor 1 and Dysregulated c-Myc Cooperatively Induce Vascular Endothelial Growth Factor and Metabolic Switches Hexokinase 2 and Pyruvate Dehydrogenase Kinase 1 (2007, background): “Particularly, in addition to its rate-limiting role in glucose metabolism, HK2 is overexpressed in most human cancers and suppresses proapoptotic molecules including Bad and Bax at the mitochondrial outer membrane, by which HK2 functions as a key coordinator by integrating glucose metabolism with ap”
Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “There are various ways in which mitochondria may regulate their own permeabilization and these originate from either the IMM or OMM.”
Akt Stimulates Aerobic Glycolysis in Cancer Cells (2004, background): “Akt has also been implicated in the regulation of glucose uptake in nontransformed cells (11, 12).”
Cytokine stimulation promotes glucose uptake via phosphatidylinositol-3 kinase/Akt regulation of Glut1 activity and trafficking. (2007, methodology): “immunofluorescence and biochemical fractionation that an activated and oncogenic form of Akt can promote accumulation of Glut1 on the surface of lymphoid cells even in the absence of cytokine (Plas et al., 2001; Rathmell et al., 2003).”
The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. (2008, background): “Second, through effects on gene expression and enzyme activity, Akt increases glycolysis and lactate production and is sufﬁcient to induce a Warburg effect in either nontransformed cells or cancer cells (Elstrom et al., 2004; Plas et al., 2001; Rathmell et al., 2003).”
Glycolysis inhibition for anticancer treatment (2006, background): “Thus, the activity of hexokinase play a key role in regulating the glucose uptake, and the activated forms of Akt have been shown to stimulate hexokinase activity (Gottlob et al., 2001; Rathmell et al., 2003).”
Exploiting the PI3K/AKT Pathway for Cancer Drug Discovery (2005, background): “AKT-induced localization of glucose transporters, including GLUT1 and GLUT3, to the cell surface and maintenance of hexokinase function in the absence of extrinsic factors might contribute to the increased ability of tumour cells to utilize external nutrient”
The activation of Akt/PKB signaling pathway and cell survival (2005, background): “In particular, the ability of Akt/PKB to promote glucose utilization can prevent the induction of conformational activation of Bax and subsequent cell apoptosis following treatment with apoptotic stimuli [103].”
Metabolic Regulation of T Lymphocytes (2013, background): “We and others have shown that Akt also promotes trafficking of the glucose transporter Glut1 to the cell surface and prevents Glut1 internalization upon activation (10, 55).”