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  • mutations
  • In this work we describe the biochemical characterization of six missense glucokinase mutations associated to MODY2 from Spanish patients, namely Y61S, V182L, C233R, E265K, A379V and K420E. (csic.es)
  • Regulation
  • The present study reiterates the accepted facts and functional significance of GK enzymology in light of "glucokinase disease" in humans and attempts to provide a perspective on the relative scientific merits of the older and newer concepts of GK regulation and how the problems might be resolved. (diabetesjournals.org)
  • Glucokinase insufficiency causes defective K ATP channel regulation, which may underlie the impaired secretion. (diabetesjournals.org)
  • The finding of two different transcription control regions in a single glucokinase gene provides a genetic basis for the tissue-specific differential regulation of glucokinase and will serve as the basis for further studies to identify and characterize the different regulatory elements and factors in the liver and β-cell, which are presumably involved. (diabetesjournals.org)
  • Given the central role of glucokinase in the regulation of insulin release, it is understandable that mutations in the GCK gene can cause both hyper and hypoglycemia. (creativebiomart.net)
  • deficiency
  • The significant abrogation of nGK −/− and nGK +/− phenotypes in the absence of K ATP demonstrate that a major factor in glucokinase deficiency is indeed altered K ATP signaling. (diabetesjournals.org)
  • Naively, both electrical triggering of secretion through K ATP channels and nonelectrical effects of glucose metabolism through ATP generation could be affected by glucokinase deficiency. (diabetesjournals.org)
  • neurons
  • In untreated primary VMH neuronal cultures, the expression of glucokinase mRNA and the number of demonstrable glucosensing neurons fell spontaneously by half over 12-96 h without loss of viable neurons. (diabetesjournals.org)
  • Transfection of neurons with small interfering glucokinase RNA did not affect survival but did reduce glucokinase mRNA by 90% in association with loss of all demonstrable glucose-excited neurons and a 99% reduction in glucose-inhibited neurons. (diabetesjournals.org)