Isozymes of glycogen synthase

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Glycogen Synthase Kinases

Extracts of rat tissues contain kinases which catalyze the conversion of glycogen synthase from the glucose 6-phosphate-independent (I) form to the glucose 6-phosphate-dependent (D) form. These kinases were stimulated by adenosine 3’:5’ monophosphate (cyclic AMP). The glycogen synthase kinase activity ratio (activity in the absence of cyclic AMP divided by activity in the presence of cyclic AMP...

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Glycogen Synthase Kinase-3

1Department of Pathology and Centre for Neuroscience, The University of Melbourne and Mental Health Research Institute, Parkville, VIC 3010, Australia 2Neurosignalling Group, Garvan Institute for Medical Research, 384 Victoria St. Darlinghurst, Sydney, NSW 2010, Australia 3Membrane Biology Group, Centre for Integrative Physiology, University of Edinburgh, George Square, Edinburgh EH8 9XD, UK 4 ...

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The Potential Role of Glycogen Synthase Kinase-3β in Neuropathy-Induced Apoptosis in Spinal Cord

Introduction: Glycogen Synthase Kinase-3β (GSK-3β) participates in several signaling pathways and plays a crucial role in neurodegenerative diseases, inflammation, and neuropathic pain. The ratio of phosphorylated GSK-3β over total GSK-3β (p-GSK-3β/t-GSK-3β) is reduced following nerve injury. Apoptosis is a hallmark of many neuronal dysfunctions in the context of neuropathic pain. Thus, this st...

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Selective loss of glycogen synthase kinase-3α in birds reveals distinct roles for GSK-3 isozymes in tau phosphorylation.

Mammalian glycogen synthase kinase-3 (GSK-3), a critical regulator in neuronal signaling, cognition, and behavior, exists as two isozymes GSK-3α and GSK-3β. Their distinct biological functions remains largely unknown. Here, we examined the evolutionary significance of each of these isozymes. Surprisingly, we found that unlike other vertebrates that harbor both GSK-3 genes, the GSK-3α gene is mi...

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Allosteric regulation of glycogen synthase controls glycogen synthesis in muscle.

Glycogen synthase (GS), a key enzyme in glycogen synthesis, is activated by the allosteric stimulator glucose-6-phosphate (G6P) and by dephosphorylation through inactivation of GS kinase-3 with insulin. The relative importance of these two regulatory mechanisms in controlling GS is not established, mainly due to the complex interplay between multiple phosphorylation sites and allosteric effecto...

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ژورنال

عنوان ژورنال: FEBS Letters

سال: 1984

ISSN: 0014-5793

DOI: 10.1016/0014-5793(84)81144-8