Search results for: Glycogen Phosphorylase, muscle
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The Hyperglycemic Effect of Melatonin in the Chinese Mitten Crab, .
Melatonin has been identified in a variety of invertebrate species, but its function is not as well understood as in crustaceans. The effects of melatonin on hemolymph glucose levels and tissue carbohydrate metabolism in the Chinese mitten crab, , were fully investigated in this study. Moreover, whether the eyestalk (an important endocrine center in invertebrate species) involves in this process or not, also were clarified. Analysis revealed that eyestalk ablation, especially bilateral, caused a significant decrease in the hemolymph glucose level. Moreover, injection of melatonin induced hyperglycemia in a dose-dependent manner both in intact and ablated crabs. Based on the expression of mRNA in the 10 different tissues, eyestalk, thoracic ganglion, intestinal tract and hemolymph were selected to estimate the effect of melatonin on the expression of mRNA. Bilateral eyestalk ablation caused a significant increase in the expression of mRNA in the thoracic ganglion, intestinal tract and hemolymph compared with the controls. In addition, injection of melatonin into intact or ablated crabs elevated the mRNA level in the eyestalk, thoracic ganglion and intestinal tract tissues compared with controls. The hemolymph mRNA after melatonin injection was elevated only in ablated crabs. Administration of melatonin resulted in a significant decrease in total carbohydrates and glycogen levels with an increase in phosphorylase activity levels in the hepatopancreas and muscle in intact and ablated crabs. Our findings demonstrated that melatonin can induce hyperglycemic effects in both intact and ablated crabs, suggesting that this effect is probably not mediated solely via eyestalk.
2998 related Products with: The Hyperglycemic Effect of Melatonin in the Chinese Mitten Crab, .
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Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells.
Glycogen synthesis by mink uterine epithelial cells is stimulated by estradiol (E ) during estrus, although the mechanism/s through which the steroid promotes glycogen accumulation are unknown. Our aim was to determine if insulin is required for E induced glycogen synthesis by an immortalized mink uterine epithelial cell line (GMMe). We show that the cells expressed the genes for glycogen metabolizing enzymes (hexokinase 1, glucose-6-phosphatase 3, glycogen synthase 1, and glycogen phosphorylase-muscle), receptors for insulin, insulin-like growth factor 1 and E (Esr1). Interestingly, treatment of cells with E alone failed to stimulate glycogen production, whereas supraphysiological concentrations of insulin (50 μg/ml) only, significantly increased glycogen content. Moreover, insulin + E increased glycogen content when compared to insulin alone (p < 0.05), an affect that was blocked when cells were treated with the pure E receptor antagonist ICI 182,780. Glycogen synthesis in response to insulin was significantly inhibited when cells were pre-treated with picropodophyllotoxin, an IGF1R antagonist. Treatment of cells with LY294002, a phosphatidylinositol 3-kinase (PI3K) antagonist, blocked insulin's effects on glycogen production whereas treatment with U0126, an inhibitor of mitogen activated kinase-kinase (MEK1/2) was without effect. These findings suggest to us that the affects of E on glycogen synthesis by GMMe cells is mediated through Esr1 and increased responsiveness of the cells to insulin. Because picropodophylotoxin blocked the effects of insulin on glycogen production, and both insulin and IGF1 act through PI3K, it is possible that IGF1 plays a role in glycogen production by these cells. 1080 related Products with: Activation of the IGF1 receptor stimulates glycogen synthesis by mink uterine epithelial cells.
anti Transferrin receptor
Human Uterine Microvascul
Dog Receptor-binding canc
Mouse Anti-Human Fibrobla
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Rat monoclonal anti mouse
Epithelial Membrane Anti
Epithelial Membrane Anti
Estrogen Receptor; Clone
Estrogen Receptor; Clone
Progesterone Receptor (P
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Synthesis of New C- and N-β-d-Glucopyranosyl Derivatives of Imidazole, 1,2,3-Triazole and Tetrazole, and Their Evaluation as Inhibitors of Glycogen Phosphorylase.
The aim of the present study was to broaden the structure-activity relationships of - and -β-d-glucopyranosyl azole type inhibitors of glycogen phosphorylase. 1-Aryl-4-β-d-gluco-pyranosyl-1,2,3-triazoles were prepared by copper catalyzed azide-alkyne cycloadditions between -perbenzylated or -peracetylated β-d-glucopyranosyl ethynes and aryl azides. 1-β-d-Gluco-pyranosyl-4-phenyl imidazole was obtained in a glycosylation of 4(5)-phenylimidazole with -peracetylated α-d-glucopyranosyl bromide. -β-d-Glucopyranosyl--substituted-tetrazoles were synthesized by alkylation/arylation of -perbenzoylated 5-β-d-glucopyranosyl-tetrazole or from a 2,6-anhydroheptose tosylhydrazone and arenediazonium salts. 5-Substituted tetrazoles were glycosylated by -peracetylated α-d-glucopyranosyl bromide to give -β-d-glucopyranosyl--substituted-tetrazoles. Standard deprotections gave test compounds which were assayed against rabbit muscle glycogen phosphorylase . Most of the compounds proved inactive, the best inhibitor was 2-β-d-glucopyranosyl-5-phenyltetrazole (IC 600 μM). These studies extended the structure-activity relationships of β-d-glucopyranosyl azole type inhibitors and revealed the extreme sensitivity of such type of inhibitors towards the structure of the azole moiety. 1744 related Products with: Synthesis of New C- and N-β-d-Glucopyranosyl Derivatives of Imidazole, 1,2,3-Triazole and Tetrazole, and Their Evaluation as Inhibitors of Glycogen Phosphorylase.
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AZD-3514 Mechanisms: Andr
17β-Acetoxy-2α-bromo-5Î
(5α,16β)-N-Acetyl-16-[2
(5α,16β)-N-Acetyl-16-ac
5α-N-Acetyl-2'H-androst-
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Elevated GLUT4 and glycogenin protein abundance correspond to increased glycogen content in the soleus muscle of mdx mice with no benefit associated with taurine supplementation.
Duchenne muscular dystrophy (DMD) patients and the dystrophic mdx mouse have an elevated demand for ATP requiring processes, including Ca regulation and skeletal muscle regeneration. As a key substrate for cellular ATP production, altered glycogen metabolism may contribute significantly to dystrophic pathology and explain reports of mild glucose intolerance. We compare the soleus and extensor digitorum longus (EDL) muscles of the mdx mouse during active muscle necrosis (at 28 days) and at 70 days where pathology is stable. We further investigate the impact of taurine (tau) on dystrophic glycogen metabolism to identify if the benefit seen with tau in a previous study (Barker et al. ) was in part owed to altered glycogen handling. The soleus muscle of 28- and 70-day-old mdx mice had elevated glucose transporter type 4 (GLUT4), glycogenin protein abundances and glycogen content compared to WT (C57BL10/ScSn) controls. Mdx tau mice exhibited modestly reduced glycogen compared to their respective mdx group. The EDL muscle of 28 days mdx tau mice had a ~70% increase in glycogenin protein abundance compared to the mdx but 50% less glycogen content. A twofold greater phosphorylated glycogen synthase (p-GS) and glycogen phosphorylase (p-GP) protein abundance was observed in the 70-day-old mdx soleus muscle than in the 28-day-old mdx soleus muscle. Glycogen debranching enzyme (GDE) protein abundance was elevated in both 28- and 70-day-old mdx soleus muscles compared to WT controls. We identified an increase in proteins associated with glucose uptake and utilization specific to the predominantly slow-twitch soleus muscle of mdx mice regardless of age and that taurine affords no obvious benefit to glycogen metabolism in the mdx mouse. 1667 related Products with: Elevated GLUT4 and glycogenin protein abundance correspond to increased glycogen content in the soleus muscle of mdx mice with no benefit associated with taurine supplementation.
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p130Cas-associated protei
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The regulation of glycogenolysis in brain.
The key regulatory enzymes of glycogenolysis are phosphorylase kinase and glycogen phosphorylase. Both enzymes are activated by phosphorylation and small ligands, and both enzymes have distinct isoforms predominantly expressed in muscle, liver or brain. This minireview examines the regulatory properties of the isoforms associated with the three tissues, focusing on potential regulatory similarities and differences. Despite the fact that the least is known about the brain isoforms, it is likely that the regulation of brain glycogenolysis has features distinct from muscle and liver. 1731 related Products with: The regulation of glycogenolysis in brain.
DNA (cytosine 5) methyltr
Beta Amyloid (42) ELISA K
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Cell Cycle Control Phosph
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A multidisciplinary study of 3-(β-d-glucopyranosyl)-5-substituted-1,2,4-triazole derivatives as glycogen phosphorylase inhibitors: Computation, synthesis, crystallography and kinetics reveal new potent inhibitors.
3-(β-d-Glucopyranosyl)-5-substituted-1,2,4-triazoles have been revealed as an effective scaffold for the development of potent glycogen phosphorylase (GP) inhibitors but with the potency very sensitive to the nature of the alkyl/aryl 5-substituent (Kun et al., Eur. J. Med. Chem. 2014, 76, 567). For a training set of these ligands, quantum mechanics-polarized ligand docking (QM-PLD) demonstrated good potential to identify larger differences in potencies (predictive index PI = 0.82) and potent inhibitors with K's < 10 μM (AU-ROC = 0.86). Accordingly, in silico screening of 2335 new analogues exploiting the ZINC docking database was performed and nine predicted candidates selected for synthesis. The compounds were prepared in O-perbenzoylated forms by either ring transformation of 5-β-d-glucopyranosyl tetrazole by N-benzyl-arenecarboximidoyl chlorides, ring closure of C-(β-d-glucopyranosyl)formamidrazone with aroyl chlorides, or that of N-(β-d-glucopyranosylcarbonyl)arenethiocarboxamides by hydrazine, followed by deprotections. Kinetics experiments against rabbit muscle GPb (rmGPb) and human liver GPa (hlGPa) revealed five compounds as potent low μM inhibitors with three of these on the submicromolar range for rmGPa. X-ray crystallographic analysis sourced the potency to a combination of favorable interactions from the 1,2,4-triazole and suitable aryl substituents in the GP catalytic site. The compounds also revealed promising calculated pharmacokinetic profiles. 1317 related Products with: A multidisciplinary study of 3-(β-d-glucopyranosyl)-5-substituted-1,2,4-triazole derivatives as glycogen phosphorylase inhibitors: Computation, synthesis, crystallography and kinetics reveal new potent inhibitors.
EnzyChromâ„¢ Kinase Assay
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Screen Questâ„¢ Membrane
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Bovine Androstenedione,AS
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Wave of renal impairment.
We present a case of a 51-year-old man who went to the emergency department after an almost-drowning episode, presenting with muscular weakness, myalgia and dark urine. Laboratory data showed a severe rhabdomyolysis (creatine kinase 497 510 U/L). Despite aggressive fluid therapy, an oliguric acute kidney injury was established with temporary need of haemodialysis. The patient had a longtime history of exercise intolerance and family history of a metabolic myopathy, namely a sister with McArdle's disease. The genetic test was positive. McArdle's disease is an autosomal recessive disorder caused by mutations in the muscle glycogen phosphorylase gene that encodes the myophosphorylase. The main symptom consists in exercise intolerance and the most severe complication is rhabdomyolysis with acute renal failure. Metabolic myopathies, such as McArdle's disease, should be considered in patients with acute renal failure due to unexplained severe rhabdomyolysis, especially if there are chronic complaints of exercise intolerance and positive family history. 1368 related Products with: Wave of renal impairment.
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Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
Rabbit Anti-Renalase Poly
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Clinical utility gene card for McArdle disease.
Name of the disease (synonyms) McArdle disease (glycogenosis type V; glycogen storage disease V (GSDV); PYGM deficiency; muscle glycogen phosphorylase deficiency; myophosphorylase deficiency). OMIM# of the disease #232600. Name of the analysed genes or DNA/chromosome segments Muscle glycogen phosphoryalse (PYGM). OMIM# of the gene(s) #608455.Review of the analytical and clinical validity as well as of the clinical utility of DNA-based testing for variants in the PYGM gene(s) in⊠diagnostic,⊠predictive and⊠prenatal settings and for⊠risk assessment in relatives. 1555 related Products with: Clinical utility gene card for McArdle disease.
TUCAN CARD8 Blocking Pept
Liver disease spectrum ti
Lung disease spectrum tis
Colon disease spectrum ti
Breast pre cancerous dise
Breast disease spectrum t
Cardiovascular disease ti
Cardiovascular disease ti
Male genitourinary system
Ovarian disease spectrum
Ovary disease spectrum (o
Skin disease tissue array
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A New Condition in McArdle Disease: Poor Bone Health-Benefits of an Active Lifestyle.
McArdle disease (muscle glycogen phosphorylase deficiency) is a genetic condition associated with exercise intolerance, but how it affects lean mass (LM) and bone mineral content (BMC) and density (BMD) in patients is unknown. We compared these variables between McArdle patients and age-/sex-matched healthy controls and assessed their potential association with physical activity levels in patients. 1786 related Products with: A New Condition in McArdle Disease: Poor Bone Health-Benefits of an Active Lifestyle.
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