2.4.1.11: glycogen(starch) synthase
This is an abbreviated version!
For detailed information about glycogen(starch) synthase, go to the full flat file.
Word Map on EC 2.4.1.11
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2.4.1.11
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kinase-3
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phosphorylase
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insulin-stimulated
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hepatocytes
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alzheimer
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3-kinase
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clamp
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mellitus
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tau
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hexokinase
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neuroprotective
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hyperglycemia
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6-phosphate
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lithium
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phosphatidylinositol
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glucose-6-phosphatase
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glycogenolysis
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amylose
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disposal
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hyperphosphorylation
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insulin-resistant
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insulin-mediated
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hyperinsulinemic
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irs-1
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waxy
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glycogenesis
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amylopectin
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licl
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adp-glucose
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niddm
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glucokinase
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soleus
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glucose-6-p
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non-insulin-dependent
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insulin-induced
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amp-dependent
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vastus
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euglycemic
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phosphatase-1
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gsk-3beta
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agpase
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debranching
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p-gsk-3
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medicine
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substrate-1
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2,6-bisphosphate
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euglycemic-hyperinsulinemic
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nonoxidative
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phosvitin
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kinase-3beta
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nutrition
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lafora
- 2.4.1.11
- kinase-3
- phosphorylase
-
insulin-stimulated
- hepatocytes
- alzheimer
- 3-kinase
-
clamp
- mellitus
- tau
- hexokinase
-
neuroprotective
- hyperglycemia
- 6-phosphate
- lithium
- phosphatidylinositol
- glucose-6-phosphatase
-
glycogenolysis
- amylose
-
disposal
-
hyperphosphorylation
-
insulin-resistant
-
insulin-mediated
-
hyperinsulinemic
- irs-1
-
waxy
-
glycogenesis
- amylopectin
- licl
- adp-glucose
- niddm
- glucokinase
- soleus
-
glucose-6-p
-
non-insulin-dependent
-
insulin-induced
-
amp-dependent
-
vastus
-
euglycemic
- phosphatase-1
- gsk-3beta
- agpase
-
debranching
-
p-gsk-3
- medicine
- substrate-1
-
2,6-bisphosphate
-
euglycemic-hyperinsulinemic
-
nonoxidative
- phosvitin
- kinase-3beta
- nutrition
- lafora
Reaction
Synonyms
Cg-GYS, GBSS, GBSSI, glucosyltransferase, uridine diphosphoglucose-glycogen, glycogen synthase, glycogen synthase 2, glycogen synthase-2, glycogen synthetase (starch), granule bound starch synthase, granule-bound starch synthase, GS-I, GSN, GSY2p, Gys-2, GYS1, GYS2, Gys2p, starch synthase I, starch/glycogen synthase, TVAG_258220, UDP-glucose-glycogen glucosyltransferase, UDP-glycogen synthase, UDPG-glycogen synthetase, UDPG-glycogen transglucosylase, uridine diphosphoglucose-glycogen glucosyltransferase
ECTree
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Activating Compound
Activating Compound on EC 2.4.1.11 - glycogen(starch) synthase
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Bile acids
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enhance the activity of the insulin receptor and glycogen synthase in primary hepatocytes
bisperoxyvanadium 1,10-phenanthroline
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phosphatidylinositol 3-kinase inhibitor wortmannin and rapamycin inhibits activation
glucose-6-phosphate
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D-glucose 6-phosphate binding structure, Arg580 forms an interaction with the 6-phosphate of D-glucose 6-phosphate, overview. The eukaryotic enzyme is activated by protein phosphatases and D-glucose 6-phosphate binding. The enzyme's response to D-glucose 6-phosphate is controlled by Arg583 and Arg587, while four additional arginine residues present within the same regulatory helix regulate the response to phosphorylation
insulin-like growth factor 1
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stimulation of activity. In patients with type 2 diabetes a significant decrease in glycogen synthase activity is accompanied by the decrease in the effect of peptides, giving the following order of their efficiency: insulin = IGF-1> relaxin. In myometrium of pregnant women with gestational treated and untreated diabetes, glycogen synthase activity decreases, the effect of insulin is weaker, whereas the effects of relaxin and IGF-1increase thus giving the following order of their efficiency: relaxin > IGF-1 > insulin. Insulin therapy of type 1 diabetes incompletely restores sensitivity of the enzymes to the peptide actions
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relaxin
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stimulation of activity. In patients with type 2 diabetes a significant decrease in glycogen synthase activity is accompanied by the decrease in the effect of peptides, giving the following order of their efficiency: insulin = IGF-1 > relaxin. In myometrium of pregnant women with gestational treated and untreated diabetes, glycogen synthase activity decreases, the effect of insulin is weaker, whereas the effects of relaxin and IGF-1 increase thus giving the following order of their efficiency: relaxin > IGF-1 > insulin. Insulin therapy of type 1 diabetes incompletely restores sensitivity of the enzymes to the peptide actions
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D-glucose
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phosphatidylinositol 3-kinase inhibitor wortmannin inhibits activation
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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glucose-6-phosphate dependent form is inactive in vivo
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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enzyme from cells cultivated in low glucose concentrations is more sensitive to glucose 6-phosphate
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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stimulates at UDP-glucose concentration of 0.4 mM
glucose 6-phosphate
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2fold activation in vivo and 10fold activation in vitro
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
glucose 6-phosphate
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synthase D, i.e. phosphorylated form, is glucose 6-phosphate dependent, synthase I, i.e. dephosphorylated form, is glucose 6-phosphate independent, interconversion of D and I forms and vice versa
Insulin
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stimulation of activity. In patients with type 1 diabetes glycogen synthase activity remains unchanged versus control, and insulin does not stimulate the enzyme activity. In patients with type 2 diabetes a significant decrease in glycogen synthase activity is accompanied by the decrease in the effect of peptides, giving the following order of their efficiency: insulin = IGF-1> relaxin. In myometrium of pregnant women with gestational treated and untreated diabetes, glycogen synthase activity decreases, the effect of insulin is weaker, whereas the effects of relaxin and IGF-1increase thus giving the following order of their efficiency: relaxin > IGF-1> insulin. Insulin therapy of type 1 diabetes incompletely restores sensitivity of the enzymes to the peptide actions
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Insulin
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phosphatidylinositol 3-kinase inhibitor wortmannin inhibits activation
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e.g. sugar phosphates, inorganic phosphate, nucleoside phosphates, activation of synthase I