ライフサイエンスコーパス: glycogen phosphorylase

1 sterically regulates the oligomeric state of glycogen phosphorylase.

2 use a rise in [AMP] is necessary to activate glycogen phosphorylase.

3 le in vivo by altering glycogen synthase and glycogen phosphorylase.

4 had no effect on either glycogen synthase or glycogen phosphorylase.

5 proteins, and is an allosteric regulator of glycogen phosphorylase.

6 h other by studying site-directed mutants of glycogen phosphorylase.

7 and catalytic properties with the mammalian glycogen phosphorylase.

8 The product of the developmentally regulated glycogen phosphorylase-2 gene (gp2) catalyzes the degrad

9 Glycogen phosphorylase a (GPa) is correlated with metabo

10 An inhibitor of human liver glycogen phosphorylase a (HLGPa) has been identified and

11 pared with vehicle infused ZDF (ZDF-V), high glycogen phosphorylase a activity was decreased and low

12 r sensitivity, and relative activity against glycogen phosphorylase a and C subunit as substrates, th

13 nt association/ dissociation equilibrium for glycogen phosphorylase A and malate dehydrogenase.

14 bilitating effects of diabetes, making liver glycogen phosphorylase a potential therapeutic target.

15 APAP showed twofold and greater increases in glycogen phosphorylase a stimulation at 6 hours, which w

16 ed by measuring Ca2+-dependent activation of glycogen phosphorylase a.

17 the active and inactive forms of human liver glycogen phosphorylase a.

18 Adrenaline infusion increased glycogen phosphorylase "a" by > 2-fold above basal level

19 in light chain, aldolase A, pyruvate kinase, glycogen phosphorylase, actinin, gamma-actin, ryanodine

20 esults demonstrate that adrenaline increased glycogen phosphorylase activation and glycolytic flux wi

21 Hyperglycemia was associated with elevated glycogen phosphorylase activity and decreased glycogen s

22 rt by a lesser forskolin-induced increase in glycogen phosphorylase activity in PTG-overexpressing ce

23 Glycogen phosphorylase activity increased in both muscle

24 en synthase activity is increased by 34% and glycogen phosphorylase activity is decreased by 17% (P <

25 hase activity was approximately 50% greater, glycogen phosphorylase activity was approximately 50% lo

26 This, combined with decreased glycogen phosphorylase activity, results in increased gl

27 thase activation state and a 40% decrease in glycogen phosphorylase activity.

28 rease in glycogen synthase and a decrease in glycogen phosphorylase activity.

29 light on the isoform-specific regulation of glycogen phosphorylase and glycogen metabolism.

30 and by down-regulation of the expression of glycogen phosphorylase and its activating kinase, phosph

31 indicated that genes encoding homologues of glycogen phosphorylase and nonphosphorylating, NADP-depe

32 sight into the temporal relationship between glycogen phosphorylase and PDC activation in vivo in ske

33 of enzymes coupling between creatine kinase, glycogen phosphorylase and sarcoplasmic reticular Ca2+ A

34 of glycogen synthase flux; (c) inhibition of glycogen phosphorylase and the activation of glycogen sy

35 enaline infusion on the activation status of glycogen phosphorylase and the pyruvate dehydrogenase co

36 dition it is suggested that creatine kinase, glycogen phosphorylase and the sarcoplasmic reticular Ca

37 f phosphorylase phosphatase, inactivation of glycogen phosphorylase, and activation of glycogen synth

38 so bind differentially to glycogen synthase, glycogen phosphorylase, and phosphorylase kinase, thereb

39 binds the PP1 substrates glycogen synthase, glycogen phosphorylase, and phosphorylase kinase.

40 binding to the multiple binding sites of the glycogen phosphorylase, and then we have investigated th

41 les, where the enzymes glycogen synthase and glycogen phosphorylase are concentrated.

42 Phosphorylation of glycogen phosphorylase at residue Ser14 triggers a confo

43 me complex that phosphorylates and activates glycogen phosphorylase b (GP b) in a Ca (2+)-dependent r

44 approach to the analysis of the kinetics of glycogen phosphorylase b (GPb).

45 to a region opposite the regulatory face of glycogen phosphorylase b (P-b), providing a probe for de

46 ype and mutant enzymes were generated, using glycogen phosphorylase b as the structural template.

47 haracterizing the self-association of muscle glycogen phosphorylase b has been reappraised.

48 ng of substrates and allosteric effectors to glycogen phosphorylase b has provided evidence that the

49 The receptor geometry of glycogen phosphorylase b, GPb, is available for structur

50 quantifying the allosteric effect of AMP on glycogen phosphorylase b.

51 understand the physical interaction between glycogen phosphorylase-b (P-b) and its only known kinase

52 sought to determine whether plasma levels of glycogen phosphorylase BB (GPBB) isoform increased in pa

53 n conversion enzymes glycogen synthase I and glycogen phosphorylase BB, dispersed throughout the type

54 ,N-diethyldithiocarbamate suggest that brain glycogen phosphorylase (bGP) and glycogen metabolism cou

55 specific reactive cysteine residues in brain glycogen phosphorylase (bGP).

56 norjirimycin tetrazole has poor affinity for glycogen phosphorylase but that phosphate substantially

57 The Ca(2+)-dependent activation of glycogen phosphorylase by PhK couples muscle contraction

58 Glycogen phosphorylases catalyze the breakdown of glycog

59 sed that the coupling of creatine kinase and glycogen phosphorylase classifies as a novel class of di

60 ing studies at 2.5 A resolution with R state glycogen phosphorylase crystals showed that the protein

61 deconstruction of known inhibitors from the glycogen phosphorylase enzyme, a therapeutic target agai

62 It also showed increased glycogen phosphorylase flux in L-G6pc(-/-) mice, which i

63 l/l per min (P = 0.018 vs. control), whereas glycogen phosphorylase flux remained unchanged (0.24 +/-

64 curred in protocol I mostly due to decreased glycogen phosphorylase flux, whereas in protocol II inhi

65 of glycogen synthase flux and inhibition of glycogen phosphorylase flux.

66 sion of unlabeled glucose to assess rates of glycogen phosphorylase flux.

67 ycogenolysis primarily through inhibition of glycogen phosphorylase flux; (b) hyperinsulinemia, per s

68 search for selective effective inhibitors of glycogen phosphorylase for the treatment of type II diab

69 med using genetic markers flanking the liver glycogen phosphorylase gene ( PYGL ), which was suspecte

70 he absence and presence of natural abundance glycogen phosphorylase, glucose-specific enzyme IIA, or

71 nd diverse superfamily that is termed GPGTF (glycogen phosphorylase/glycosyl transferase).

72 ase activity in P-HFF versus P and increased glycogen phosphorylase (GP) activity in both P (1.7-fold

73 ral similarity between the catalytic core of glycogen phosphorylase (GP) and BGT, we have modelled th

74 In animals, glycogen phosphorylase (GP) exists in an inactive (T sta

75 we have studied 10 site-directed mutants of glycogen phosphorylase (GP) in its amino-terminal regula

76 perimental evaluation of the contribution of glycogen phosphorylase (GP) to biochemical pathways is l

77 Glycogen phosphorylase (GP), a key enzyme in glycogen me

78 ibitors against muscle and liver isoforms of glycogen phosphorylase (GP).

79 ; the protein was subsequently identified as glycogen phosphorylase (GP).

80 m of local protein refolding activates yeast glycogen phosphorylase (GP).

81 GMPMT was compared with glycogen phosphorylase (GP).

82 ity by the UPR was detected, AMP-independent glycogen phosphorylase (GP).

83 Glucose analogue inhibitors of glycogen phosphorylase, GP, may be of clinical interest

84 ified three candidate structural homologues: glycogen phosphorylase (gpb), a 70 kDa soluble lytic tra

85 f a set of 47 glucose analogue inhibitors of glycogen phosphorylase (GPb).

86 S. cerevisiae, neutral trehalase (Nth1) and glycogen phosphorylase (Gph1), and show that their activ

87 Interest in the kinetics of glycogen phosphorylase has recently been renewed by the

88 mitochondrial creatine phosphokinase, muscle glycogen phosphorylase, hexokinase I, muscle phosphofruc

89 itro Vmax values with in vivo flux rates for glycogen phosphorylase, hexokinase, and phosphofructokin

90 Levels of glycogen phosphorylase in these muscles increased (up to

91 with hyperglycemia to directly hyperinhibit glycogen phosphorylase, in turn blocking glycogenolysis

92 To investigate this possibility, we used a glycogen phosphorylase inhibitor (BAY R3401) to inhibit

93 . min(-1)) were measured with and without a glycogen phosphorylase inhibitor (GPI) using [2-(3)H]glu

94 Glucose was lowered using a glycogen phosphorylase inhibitor and a low dose of insul

95 olysin zinc protease inhibitor dataset and a glycogen phosphorylase inhibitor dataset.

96 hypoglycemia achieved by administration of a glycogen phosphorylase inhibitor results in increased gl

97 min), during which BAY R 3401 (10 mg/kg), a glycogen phosphorylase inhibitor, was administered orall

98 0 min), during which BAY R3401 (10 mg/kg), a glycogen phosphorylase inhibitor, was administered orall

99 of the test period, Bay R3401 (10 mg/kg), a glycogen phosphorylase inhibitor, was administered orall

100 Catalysis by glycogen phosphorylase involves a mechanism in which bin

101 Glycogen phosphorylase is a key enzyme in the regulation

102 Glycogen phosphorylase is a muscle enzyme which metaboli

103 Glycogen phosphorylase is found in resting muscle as pho

104 Glycogen phosphorylase is the key enzyme that breaks dow

105 and consists of three isoenzymes, including glycogen phosphorylase isoenzyme BB (GPBB).

106 In the brain, both muscle and brain glycogen phosphorylase isozymes regulate glycogen mobili

107 Glycogen phosphorylase kinase activates glycogen phospho

108 s in a dominant manner to completely inhibit glycogen phosphorylase kinase enzyme activity and that t

109 a mutation in the catalytic subunit of liver glycogen phosphorylase kinase in a patient with Mauriac

110 e patient's mother possessed the same mutant glycogen phosphorylase kinase subunit, but did not have

111 ma membrane Ca-ATPase, a MARCKS homolog, and glycogen phosphorylase kinase were assessed using freque

112 ng phospholamban, troponin I, C protein, and glycogen phosphorylase kinase.

113 nt degradation of phosphoglycerate mutase 2, glycogen phosphorylase muscle form, pyruvate kinase musc

114 the active form of Rac 1 GTPase binds to the glycogen phosphorylase muscle isoform (PYGM) and modulat

115 In mammalian glycogen phosphorylase, phosphorylation occurs at a dist

116 iabetic properties due to enzyme inhibition (glycogen phosphorylase, protein tyrosine phosphatase 1B)

117 nolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate carbo

118 d by mass spectrometry the muscle isoform of glycogen phosphorylase (PYGM) as a novel Rac1 effector m

119 carbonylation of protein spots identified as glycogen phosphorylase, pyruvate kinase muscle isozyme,

120 Deletion of glgB or glgP (glycogen phosphorylase) resulted in defective growth and

121 e classic regulatory enzymes, hexokinase and glycogen phosphorylase, show significant drops in flight

122 le nucleotide polymorphisms (SNPs) in muscle glycogen phosphorylase showed evidence of association wi

123 Kinetic studies with glycogen phosphorylase showed that nojirimycin tetrazole

124 in the active sites of glycogen synthase and glycogen phosphorylase support the idea of a common cata

125 s mechanism utilizes the rapid conversion of glycogen phosphorylase, the "fight-or-flight" enzyme, to

126 Glycogen phosphorylase kinase activates glycogen phosphorylase, the enzyme that catalyzes the fi

127 blood glucose levels physiologically inhibit glycogen phosphorylase to diminish glucose release from

128 During early ischemia, conversion of glycogen phosphorylase to the a or "active" form was les

129 phosphoglycerate mutase 2, beta enolase and glycogen phosphorylase), transport proteins (fatty acid-

130 cludes the apolipoprotein C3 cluster, muscle glycogen phosphorylase, two insulin-dependent diabetes l

131 luding proteins with known structure such as glycogen phosphorylase, UDP-GlcNAc 2-epimerase, and the

132 Alpha skeletal actin, glycogen phosphorylase, unnamed protein product (UNP) si

133 dies, the flux through glycogen synthase and glycogen phosphorylase was 0.31 +/- 0.06 and 0.17 +/- 0.

134 -288) located near the active site of muscle glycogen phosphorylase was investigated.

135 , calpastatin, cathepsin B, cathepsin L, and glycogen phosphorylase were not altered.

136 ly, the expression of the degradative enzyme glycogen phosphorylase, which is encoded by glgY, was fo