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Hexokinase 1

Hexokinases phosphorylate glucose to produce glucose-6-phosphate, the first step in most glucose metabolism pathways. This gene encodes a ubiquitous form of hexokinase which localizes to the outer membrane of mitochondria. Mutations in this gene have been associated with hemolytic anemia due to hexokinase deficiency. Alternative splicing of this gene results in five transcript variants which encode different isoforms, some of which are tissue-specific. Each isoform has a distinct N-terminus; the remainder of the protein is identical among all the isoforms. A sixth transcript variant has been described, but due to the presence of several stop codons, it is not thought to encode a protein. [provided by RefSeq, Apr 2009] (from NCBI)
Papers using Hexokinase antibodies
A membrane protein complex mediates retro-translocation from the ER lumen into the cytosol
Ng Davis T.W. et al., In The Journal of Cell Biology, 2003
... Anti-hexokinase antibody was purchased from United States Biological Inc ...
High glucose-induced oxidative stress and mitochondrial dysfunction in neurons.
Bush Ashley I., In PLoS ONE, 2001
... Goat polyclonal anti-cytochrome c oxidase and monoclonal anti-hexokinase-1 antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA) ...
Papers on Hexokinase
Mitochondrial detachment of hexokinase 1 in mood and psychotic disorders: implications for brain energy metabolism and neurotrophic signaling.
Fiskum et al., Baltimore, United States. In J Psychiatr Res, 2012
This study proposed that HK1 mitochondrial detachment could be linked to these disorders through impaired energy metabolism, increased vulnerability to oxidative stress, and impaired brain growth and development.
Studies of a genetic variant in HK1 in relation to quantitative metabolic traits and to the prevalence of type 2 diabetes.
Pedersen et al., Copenhagen, Denmark. In Bmc Med Genet, 2010
An association is noted between the rs7072268 T-allele in HK1 and an increased blood glucose in non-diabetic individuals and a nominal association with type 2 diabetes prior to Bonferroni correction.
A soluble form of the pilus protein FimA targets the VDAC-hexokinase complex at mitochondria to suppress host cell apoptosis.
Yu et al., Singapore, Singapore. In Mol Cell, 2010
FimA strengthens the VDAC1-hexokinase(I and II) interaction and prevents dissociation of hexokinase from VDAC1 triggered by apoptotic stimuli.
Amyloid-β triggers the release of neuronal hexokinase 1 from mitochondria.
De Felice et al., Rio de Janeiro, Brazil. In Plos One, 2009
Abeta-induced cellular redistribution and inactivation of neuronal HKI play important roles in oxidative stress and neurodegeneration in Alzheimer's disease
Genetic variant in HK1 is associated with a proanemic state and A1C but not other glycemic control-related traits.
Froguel et al., Lille, France. In Diabetes, 2009
HK1 may influence A1C levels through its anemic effect or its effect on glucose metabolism in erythrocytes, which may have implications for type 2 diabetes diagnosis and care.
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