BAD and glucokinase reside in a mitochondrial complex that integrates glycolysis and apoptosis

By N. Danial, C. Gramm, L. Scorrano, Chen-Yu Zhang, S. Krauss, A. Ranger, Sandeep R. Datta, Michael E. Greenberg, L. Licklider, Bradford B. Lowell and 2 more. Nature, 2003

740 citations recorded by the source corpus.

Subfields: Cell Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/bc0ed13706d5bc55dcbb30937c078a548fa5b67d

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Citations in the corpus

Glycolysis inhibition for anticancer treatment (2006, background): “Dephosphorylation of BAD at Ser-112 is associated with re-localization of BAX to mitochondria, cytochrome c release, and apoptosis (Xu et al., 2005b).”
Autophagy in metazoans: cell survival in the land of plenty (2005, background): “The importance of constitutive TCA activity in autophagic cells is supported by studies showing that providing cells with pyruvate, a TCA substrate, can suppress autophagy and can maintain cell viabilit”
Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels (2006, background): “…homologue of grp75 is part of the protein import motor associated with TIM23 in the mitochondrial matrix (Neupert and Brunner, 2002), but it was also found in the cytosol and in OMM-associated high molecular weight protein complexes (Ran et al., 2000; Danial et al., 2003; Zahedi et al., 2006).”
Mitochondrial membrane permeabilization in cell death. (2007, background): “The metabolites sharing direct antiapoptotic effects on the PTPC embrace the following: 1) ADP and ATP, which act by binding to and inhibiting ANT (53, 798); 2) creatine and cyclocreatine, through the modulation of creatine kinase (183); 3) glucose, which favors the antiapoptotic interaction between”
Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling. (2006, background): “Mitochondria are crucial organelles in intermediate metabolism and energy production (Danial et al., 2003), Ca signaling (Rizzuto et al.”
OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, neutral): “Percoll-purified normal and cBID-treated, CHAPS-solubilized mouse liver mitochondria displayed very similar elution patterns from Superose 6 columns (not shown) (Danial et al., 2003).”
The biological impact of mass-spectrometry-based proteomics (2007, background): “A mitochondrial protein complex that links apoptosis and glycolysis Stanley Korsmeyer and colleague”
Hexokinase II: Cancer's double-edged sword acting as both facilitator and gatekeeper of malignancy when bound to mitochondria (2006, background): “A recent study has also indicated that in liver cells a complex between glucokinase (the high Km isozyme among HKs that is predominantly expressed in the liver, and long known to be cytoplasmic) and Bad exists that is bound to the mitochondria (Danial et al., 2003).”
During autophagy mitochondria elongate, are spared from degradation and sustain cell viability (2011, neutral): “Primary hepatocytes were isolated as described previousl”
Growth factor regulation of autophagy and cell survival in the absence of apoptosis. (2005, background): “…growth and division cease, and prodant regulators of apoptosis and extracellular signals grammed cell death is initiated through the intrinsic miare no longer necessary to suppress mitochondrial inititochondrial pathway (Danial et al., 2003; Green and Reed, ation of apoptosis in Bax / Bak / cells.”
Sugar for the brain: the role of glucose in physiological and pathological brain function (2013, background): “Interestingly, glucokinase (GK; Glossary) is expressed in select neuronal populations in hypothalamic glucose-sensing formations [65], and a protein complex containing GK and BAD (Bcl-2 antagonist of cell death) might regulate peripheral [66], as well as central glucose sensing.”
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”