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
2.4.1.11 glycogen(starch) synthaseAdvanced search results
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Source Tissue on EC 2.4.1.11 - glycogen(starch) synthase
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SOURCE TISSUE 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
SOURCE
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synthetic peroxisome proliferator-activated receptor beta/delta, and gamma agonists markedly up-regulate Gys-2 mRNA and protein expression in mouse 3T3-L1 adipocytes
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hypoxia activates glycogen synthase in fed rat myocardium through a combination of rapid glycogenolysis, elevated local glucose 6-phosphate content, and increased protein phosphatase 1 activity, and fasting attenuates this action independent of local glucose 6-phosphate content. Activation of glycogen synthase in myocardium induced by intermittent hypoxia is much lower in fasted than in fed rats
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strong expression, relative levels of Cg-GYS transcripts appear highest in October corresponding to glycogen storage and resting period
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strong expression, relative levels of Cg-GYS transcripts appear highest in October corresponding to glycogen storage and resting period
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glycolytic glioma cells with active glycogen synthase are sensitive to phosphatase and tensin homolog (PTEN) and inhibitors of phosphatidylinositol-3 kinase and gluconeogenesis
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in distal tubular cells, adiponectin through luminal ADIPOR1 activates AMPK, leading to the inhibition of glycogen synthase. During hyperglycemia, this regulation is altered, which may explain, at least in part, the accumulation of large glycogen deposits
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glycolytic glioma cells with active glycogensynthase are sensitive to phosphatase and tensin homolog (PTEN) and inhibitors of phosphatidylinositol-3 kinase and gluconeogenesis
additional information
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expression of Gys-2 is significantly reduced in adipose tissue of peroxisome proliferator-activated receptor alpha-/-, peroxisome proliferator-activated receptor beta/delta-/- and peroxisome proliferator-activated receptor gamma+/- mice
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5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside positively regulates glycogen synthase activity and LDL receptor expression through Raf-1/MEK/p42/44MAPK/p90RSK/GSK-3 signaling cascade
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insulin receptor substrate (IRS) protein 1 knockdown reduces the glycogen synthase activity in parental HepG2 cells. It is upregulated in HepG2-CA-Akt/PKB cells
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upon rapamycin treatment, the overexpression of constitutively active Akt-1 in Hep-G2 cells leads to an increase in the phosphorylation of Akt (Ser 473) and, an increase in the GS and PP-1 activities, in contrast to a decrease in Akt phosphorylation and GS and PP-1 activities in parental HepG2 cells
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reduction in glucose production in primary hepatocytes by the overexpression of the mutant GYS2. The elevation of liver glycogen synthase activity in primary hepatocytes reduces glucose production by shunting gluconeogenic precursors into glycogen rather than by stimulating direct glucose incorporation into glycogen
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basal glycogen synthase activity in muscle lacking rictor is increased to that of insulin-stimulated controls. A decrease in basal levels of phosphorylated glycogen synthase at a GSK-3/protein phosphatase 1 (glycogen-associated protein phosphatase 1)-regulated site in rictor knockout muscle is observed. This change in glycogen synthase phosphorylation is associated with an increase in the catalytic activity of glycogen-associated glycogen-associated protein phosphatase 1 but not increased GSK-3 inactivation
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contraction activates glycogen synthase in muscles from dexamethasone-treated rats
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in low glycogen, basal and insulin-stimulated glycogen synthesis and glycogen synthase activation is higher and glycogen synthase phosphorylation (Ser645, Ser649, Ser653, Ser657) lower than in normal glycogen. Muscles with high glycogen show lower insulin-stimulated glycogen synthesis and glycogen synthase activation than normal glycogen despite similar dephosphorylation
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of insulin-resistant, fat-fed rats and chow-fed controls, either maintained in the basal state or after a euglycaemichyperinsulinaemic clamp
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elevated glycogen synthase activity in Polysaccharide Storage Myopathy horses. A gain of function mutation in GYS1 results in a glycogenosis
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slowtwitch (soleus) and fast-twitch (epitrochlearis) muscle. Improved insulin-stimulated glucose uptake and glycogen synthase activation after adrenaline infusion
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sucrose feeding does not alter muscle glycogen concentration but provokes a small reduction in the glycogen synthase activity ratio (-/+ glucose-6-phosphate) in red but not in white gastrocnemius. Dexamethasone administration augments glycogen concentration and reduces glycogen synthase activity ratio in both muscle fiber types
longissimus dorsi muscle, high expression level of GYS1
additional information
tissue distribution in tissues from the developmental stages from the first-instar larvae to fifth-instar to pupae and expression pattern, overview
additional information
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tissue distribution in tissues from the developmental stages from the first-instar larvae to fifth-instar to pupae and expression pattern, overview
additional information
tissue expression pattern of GYS1, GYS1 is upregulated during porcine myogenic cell differentiation
additional information
tissue expression pattern of GYS1, GYS1 is upregulated during porcine myogenic cell differentiation
additional information
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tissue expression pattern of GYS1, GYS1 is upregulated during porcine myogenic cell differentiation
