Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak.

By Nathan D. Majewski, V. Nogueira, Prashanth T. Bhaskar, Platina E. Coy, Jennifer E. Skeen, Kathrin Gottlob, Navdeep S. Chandel, Craig B. Thompson, R. Robey, N. Hay. Molecules and Cells, 2004

661 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/6e4f09a1debfdf6c8d566b36a999f35458fe47cf

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Citations in the corpus

Tumor glycolysis as a target for cancer therapy: progress and prospects (2013, positive): “provides survival advantage to cancer cells [43,44].”
Sugar for the brain: the role of glucose in physiological and pathological brain function (2013, background): “HKII restricts or inhibits apoptosis in a variety of different cell types depending on whether or not it is bound to mitochondria [72, 74], and on the availability of glucose [72].”
Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, background): “The two high-affinity hexokinases, HK1 and HK2, are associated with mitochondria and were also implicated in cell survival (Gottlob et al., 2001; Majewski et al., 2004).”
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.”
Mitochondrial tumour suppressors: a genetic and biochemical update (2005, background): “Once induced, glycolytic enzymes could regulate other cellular processes that include the blocking of apoptosi”
Mitochondrial mutations in cancer (2006, background): “The binding of hexokinase II to VDAC also stabilizes the mtPTP and inhibits induction of apoptosis (Pedersen et al., 2002; Gatenby and Gillies, 2004) by antagonizing the pro-apoptotic action of Bax and Bak (Gottlob et al., 2001; Birnbaum, 2004; Majewski et al., 2004a, b).”
Targeting metabolic transformation for cancer therapy (2010, background): “and altering the expression or localization of glycolytic enzymes such as hexokinase and the family of 6-phosphofructo-2-kinase/fructose-2,6-biphosatases (PFKFBs”
Targeting mitochondria for cancer therapy (2010, background): “HK interacts with the PTPC in healthy cells, thereby inhibiting mitochondrial membrane permeabilizatio”
Hexokinase II: Cancer's double-edged sword acting as both facilitator and gatekeeper of malignancy when bound to mitochondria (2006, background): “Finally, ectopic expression of only the Nterminal domain of HK II, which alone can maintain its catalytic activity and contains the mitochondrial-binding domain, can still antagonize tBID (Majewski et al., 2004b).”