Isozymes of mammalian hexokinase: structure, subcellular localization and metabolic function

By John Eric Wilson. Journal of Experimental Biology, 2003

1,094 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/15dadef761d1f89aaa0eda74b0c2e83d63c3110e

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Citations in the corpus

Hexokinase II: Cancer's double-edged sword acting as both facilitator and gatekeeper of malignancy when bound to mitochondria (2006, background): “Interestingly, most normal mammalian tissues express very little HK II with those from muscle, adipocytes and lung expressing low but significant levels (Wilson, 1995, 2003).”
Supply and Demand in Cerebral Energy Metabolism: The Role of Nutrient Transporters (2007, background): “Interestingly, peripheral sites of GLUT3 expression include sperm, platelets, placenta, and certain human gliomas; all cell types that exhibit high rates of glucose metabolism (see Joost and Thorens, 2001; Uldry and Thorens, 2004; Wood and Trayhurn, 2003).”
Aerobic glycolysis: meeting the metabolic requirements of cell proliferation. (2011, positive): “There are four known mammalian hexokinase isoforms (HK I-IV), and HK I is expressed in most normal cells and at particularly high levels in brain tissue (Wilson 2003).”
Hexose kinases and glucose transport in the yeast Hansenula polymorpha (2005, background): “Vertebrates have four isoforms of hexokinase (Cárdenas, 1998; Wilson, 2003).”
Mitochondria in cancer cells: what is so special about them? (2008, positive): “By contrast, the type III isozyme lacks the hydrophobic N-terminal sequence known to be crucial for the binding of type I and type II isozymes to mitochondria [ 49 ].”
Nutrient sensing and signaling in the yeast Saccharomyces cerevisiae (2014, background): “, 1993), which functionally resembles the well-known product inhibition of mammalian hexokinase by glucose-6-phosphate (Wilson, 2003).”
Sugar for the brain: the role of glucose in physiological and pathological brain function (2013, background): “The Km (half-saturation constant) of HKI for glucose is very low [19], and HKI can therefore operate at maximal velocity as long as the intracellular glucose exceeds about 0.”
Glycolysis inhibition for anticancer treatment (2006, background): “At the protein level, hexokinases are either free in the cytosol or bound to the mitochondrial outer membrane (Wilson, 2003).”
Hexokinase 2 is required for tumor initiation and maintenance and its systemic deletion is therapeutic in mouse models of cancer (2013, background): “The two catalytic domains of HK2 have different kinetics properties and thus may retain its activity under conditions that are inhibitory for the single catalytic domain of HK1 (Wilson, 2003).”