Literature summary for 2.7.1.1 extracted from

Markwardt, M.L.; Seckinger, K.M.; Rizzo, M.A.
Regulation of glucokinase by intracellular calcium levels in pancreatic beta cells (2016), J. Biol. Chem., 291, 3000-3009.

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
betaTC-3 cell	-	Mus musculus	-
MIN-6 cell	-	Mus musculus	-

General Information

General Information	Comment	Organism
physiological function	inhibiting Ca2+ release from the endoplasmic reticulum decouples glucokinase activation from receptor stimulation. Pharmacological release of endoplasmic reticulum Ca2+ stimulates activation of a glucokinase optical biosensor and potentiates glucose metabolism. An optimized glucokinase biosensor using circularly permuted mCerulean3 proteins sensitively reports activation in response to insulin, glucagon-like peptide 1, and agents that raise cAMP levels. Transient, glucose-stimulated glucokinase activation is observed in TC3 and MIN6 cells. Half-maximal activation of the FRET-glucokinase sensor is estimated to occur at400 nM Ca2+. When expressed in islets, fluctuations in glucokinase activation are observed in response to glucose, and posttranslational activation of GCK enhances glucose metabolism by about 35%	Mus musculus

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Release 2023.1 (January 2023)