Glycogen phosphorylase is regulated by both allosteric control and by phosphorylation.. Hormones such as epinephrine, insulin and glucagon regulate glycogen phosphorylase using second messenger amplification systems that are linked to G proteins. Glucagon activates adenylate cyclase through a seven transmembrane receptor coupled to Gs which, in turn, activates adenylate cyclase to increase intracellular concentrations of cAMP. cAMP binds to and releases an active form of protein kinase A (PKA). Next, PKA phosphorylates phosphorylase kinase, which, in turn, phosphorylates glycogen phosphorylase b, transforming it into the active glycogen phosphorylase a. This phosphorylation is added onto the glycogen phosphorylase b serine 14. In the liver, glucagon activates another G-protein-linked receptor that triggers a different cascade, resulting in the activation of Phospholipase C (PLC). PLC indirectly causes the release of calcium from the hepatocytes endoplasmic reticulum into the cytosol. The ...
Potato phosphorylase is able to synthesize linear polyglucans from maltoheptaose primers. By coupling maltoheptaose to butane diamine, tris(2-aminoethyl)amine and amine functionalized amine functionalized poly ethyleneglycol (PEG), new primer molecules became available. The resulting di-, tri- and macro-primers were incubated with potato phosphorylase and glycogen branching enzyme from Deinococcus geothermalis. Due to the action of both enzymes, hyperbranched polyglucan arms were grown from the maltoheptaose derivatives with a maximum degree of branching of 11%. The size of the synthesized hyperbranched polyglucans could be controlled by the ratio monomer over primer. About 60%-80% of the monomers were incorporated in the glycoconjugates. The resulting hyperbranched glycoconjugates were subjected to Dynamic Light Scattering (DLS) measurements in order to determine the hydrodynamic radius and it became obvious that the structures formed agglomerates in the range of 14-32 nm.
TY - JOUR. T1 - Human brain glycogen phosphorylase. T2 - characterization of fetal cDNA and genomic sequences. AU - Gelinas, Richard P.. AU - Froman, Byron E.. AU - McElroy, Fred. AU - Tait, Robert C.. AU - Gorin, Fredric A. PY - 1989. Y1 - 1989. N2 - Glycogen phosphorylase (α-1,4-d-glucan:orthophosphate d-glucosyltransferase, EC 2.4.1.1) is the rate-determining enzyme catalyzing glycogen degradation. Human brain has been demonstrated previously to express genes of both the liver and muscle isozymes of glycogen phosphorylase. In this report, a human fetal brain cDNA and genomic DNA corresponding to the brain isozyme of glycogen phosphorylase were isolated and characterized. Transcripts corresponding to this isozyme are present in human adult and fetal brain, and at low levels in other human fetal tissues. The predicted C-terminal sequence of the protein encoded by this cDNA and gene differ from that encoded by a phosphorylase cDNA isolated from a human astrocytoma cell line.. AB - Glycogen ...
The action of nine sympathomimetic amines on contractility and on phosphorylase a and total phosphorylase activity of the isolated perfused rat heart has been studied. The following observations have been made. 1) The sympathomimetic amines with a positive inotropic action on the heart caused an increase in phosphorylase a activity of the myocarclium, hut did not change total phosphorylase activity. 2) Sympathomimetic amines with no action on the contractility of the heart had no effect on phosphorylase a activity. 3) With each drug studied there was a correlation at all drug concentrations between the increase in systolic isometric tension and the increase of phosphorylase a activity. 4) Linear log dose-response curves were obtained in studies of the action of epinephrine, norepinephrine and isoproterenol on phosphorylase a activity. 5) The structure-activity relationship of the nine drugs was the same for their ability to increase the force of contraction and for their action on phosphorylase. ...
Glycogen Phosphorylase: An enzyme that catalyzes the degradation of GLYCOGEN in animals by releasing glucose-1-phosphate from the terminal alpha-1,4-glycosidic bond. This enzyme exists in two forms: an active phosphorylated form ( PHOSPHORYLASE A) and an inactive un-phosphorylated form (PHOSPHORYLASE B). Both a and b forms of phosphorylase exist as homodimers. In mammals, the major isozymes of glycogen phosphorylase are found in muscle, liver and brain tissue.
Approximately one billion people worldwide are homozygous for a stop codon polymorphism in the ACTN3 gene (R577X) which results in complete deficiency of the fast fibre muscle protein α-actinin-3. ACTN3 genotype is associated with human athletic performance and α-actinin-3 deficient mice [Actn3 knockout (KO) mice] have a shift in the properties of fast muscle fibres towards slower fibre properties, with increased activity of multiple enzymes in the aerobic metabolic pathway and slower contractile properties. α-Actinins have been shown to interact with a number of muscle proteins including the key metabolic regulator glycogen phosphorylase (GPh). In this study, we demonstrated a link between α-actinin-3 and glycogen metabolism which may underlie the metabolic changes seen in the KO mouse. Actn3 KO mice have higher muscle glycogen content and a 50% reduction in the activity of GPh. The reduction in enzyme activity is accompanied by altered post-translational modification of GPh, suggesting ...
ddn:DND132_3085 K16153 glycogen phosphorylase/synthase [EC:2.4.1.1 2.4.1.11] , (GenBank) alpha-glucan phosphorylase (A) MDKSWLFEVSWEVCNKVGGIYTVISSKAPQAKAAFDNRYVAVGPLLDRNPGFLPSDPPDT VRPALERLKAWGIETATGQWDIPGKPLVLLIGFRNAFPAHDKLLFQLWNDYGVDSMAGGW DYIEPVLFSTAAAMAIKEISEDVGEGADVYAHFHEWMSGAGVLHLKKHAPSVSTVLTTHA TMLGRAMSGAGVDIYKRLEEIEPSQEAKAYGVTAKHSMESVSAREADCFTTVSNITRREA SNLLGTNPAVVTVNGFNLDGFADPTAVAQTRKRSRKQLLDLAANFLERDLDPAKTLLVAT SGRYEFHNKGIDLLLDGLGDLNEELAKSGKDVTVVAFLLVSCGYAGFSDEARRRLKQERY DIEKYAGISTHHLGDADHDPVVMKCRERKLDNEAVNRCCVIFIPVYLDGNDGVLNLEYYD ALAGMDLTVFPSFYEPWGYTPMESAAFAVPTVTSDRAGFGQWIMERHPQGHPGVHVLNRL EDDYETARENLALYLSDFTRWTPEERVSRSKEARKIAEEATWAHFYPRYLEAYEYAADIR TERIAGVQRMVAAPGAEISFSGVNTTQPRLRSFTVVTELPAPLARLRDVAENLWWVWHRD SQELFEWMDADKWHESGHNPVLFLDTMRRDRLAELADDPEFIGRLNSVLERFDAYMAESA KADVRGITWKNPVAYFSMEFGLHEAIPVYSGGLGLLSGDHIKSASDLNLPFIGISLLYKN GFFHQRINGNGDQVVEYHENNFATMPITPLQRNDEKVMITVDLPGRTVYAQIWEVHVGRA RLYLLDTDVVENSRSDRDITSKLYDPTSKGRIEQEIILGVGGIRLFTALDIVPSVYHLNE ...
Finding an accurate method for estimating the affinity of protein ligands activity is the most challenging task in computer-aided molecular design. In this study we investigate and compare seven diffe
contains similarity to Pfam domain PF00343 (Carbohydrate phosphorylase)contains similarity to Interpro domains IPR011833 (Glycogen/starch/alpha-glucan phosphorylase), IPR000811 (Glycosyl transferase, family 35 ...
Evidence has been presented for the existence in rat liver of P2-purinoceptors which are involved in the control of glycogenolysis. Isolated rat hepatocytes and purified liver plasma membranes have been used to study the binding of the ATP analogue adenosine 5′-[alpha- [35S]thio]triphosphate (ATP alpha [35S]) to these postulated P2-purinoceptors. The nucleotide analogue behaves as a full agonist for the activation of glycogen phosphorylase in isolated hepatocytes, 0.3 microM being required for half-maximal activation. Specific binding of ATP alpha [35S] to hepatocytes and plasma membranes occurs within 1 min and is essentially reversible. The analysis of the dose-dependency at equilibrium indicates the presence of binding sites with Kd of 0.23 microM with hepatocytes and Kd of 0.11 microM with plasma membranes. The relative affinities of 10 nucleotide analogues were deduced from competition experiments for ATP alpha [35S] binding to hepatocytes, and these correlated highly with their ...
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Chlorine atom in PDB 1c8k: Flavopiridol Inhibits Glycogen Phosphorylase By Binding At the Inhibitor Site
There are three known isozymes of the homodimeric glycogen phosphorylase (GP), liver (GP-LL), muscle (GP-MM), and brain (GP-BB). The observation that astrocytes from astroglia-rich primary cultures contain GP-BB, whereas astrocytes accompanying cultured neurons lacked this enzyme, led to the question of how the transcription of GP-BB is regulated. C6-BU-1 rat glioma cells were shown by both Western blot analysis and immunocytochemistry to express GP-BB. Since these cells express GP-BB and therefore must contain transcription factors for its transcriptional regulation, they were chosen as a model for this investigation. C6-BU-1 cells, however, turned out to be transfected by plasmids only with low efficiency. Therefore, lentiviral vectors were designed as more promising tools for the transfection of these cells. The lentiviral constructs were devised to contain two expression cassettes for integration into the host genome. Secreted alkaline phosphatase (SEAP) was placed under the control of a CMV ...
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We propose that a combination of laminaribiose and β-1,3-oligoglucan phosphorylases could be used for a one-pot enzymatic synthesis of β-1,3-oligosaccharides starting from readily available starting materials, glucose and glucose-1-phosphate. Thus, enzymatic synthesis could provide an effective way of producing designer β-1,3-oligosaccharides, compounds which potentially have several biotechnological application. However, successful biotechnological application of phosphorylases is hampered by rather limited availability of these enzymes, in fact only a small number of organisms has proven to possess enzymes with β-1,3-glucan phosphorylase activity. Our goal is to uncover potential candidates capable of demonstrating such activities and test them in practical applications. In order to achieve this goal we have undertaken research which is based on several approaches:. ...
Phosphorylase is an important allosteric enzyme in carbohydrate metabolism. Enzymes from different sources differ in their regulatory mechanisms and in their natural substrates. However, all known phosphorylases share catalytic and structural properties.
Anti-glycogen phosphorylase antibodiesGlycogen phosphorylase (EC 2.4.1.1) is an enzyme which is catalyzing the rate limiting step in the degradation of glycogen in animals by releasing glucose-1-phosphate from the terminal alpha1,4-glycosidic bond.
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Gene target information for Pygb - brain glycogen phosphorylase (house mouse). Find diseases associated with this biological target and compounds tested against it in bioassay experiments.
Enzimler E-kitap okumak için tıklayın İçindekiler Enzimlerin kimyasal yapıları Enzimlerin tesir mekanizması Aktivatörler Spesifik İon Aktivatörleri Koenzimler İnhibitörler Non kompetetif inhibitörler Kompetitif inhibitörler Diğer inhibitörler Enzimatik reaksiyonların hızı üzerine tesir eden faktörler Enzim konsantrasyonu Substrat konsantrasyonu pH hidrogen ion konsantrasyonu Isı Reaksiyon ürünleri Kofaktör konsantrasyonu ve diğer fiziksel faktörler Zaman Enzimatik […]. ...
Per-O-acetylated beta-D-glucopyranosyl azide was transformed into an intermediate iminophosphorane by PMe(3) which was then acylated to N-acyl-beta-D-glucopyranosylamines. The same azide and substituted acetylenes gave 1-(beta-D-glucopyranosyl)-4-substituted-1,2,3-triazoles in Cu(I)-catalyzed azide-alkyne cycloadditions. Deprotection of these products by the Zemplen method furnished beta-D-Glc(p)-NHCO-R derivatives as well as 1-(beta-D-Glc(p))-4-R-1,2,3-triazoles which were evaluated as inhibitors of rabbit muscle glycogen phosphorylase b. Pairs of amides versus triazoles with the same R group displayed similar inhibition constants. X-ray crystallographic studies on the enzyme-inhibitor complexes revealed high similarities in the binding of pairs with R = 2-naphthyl and hydroxymethyl, while for the R = Ph and 1-naphthyl compounds a different orientation of the aromatic part and changes in the conformation of the 280s loop were observed. By this study new examples of amide-1,2,3-triazole ...
Background Mutations in the PYGM gene encoding skeletal muscle glycogen phosphorylase (GP) cause a metabolic disorder known as McArdles disease. Previous studies in muscle biopsies and cultured muscle cells from McArdle patients have shown that PYGM mutations abolish GP activity in skeletal muscle, but that the enzyme activity reappears when muscle cells are in culture. The identification of the GP isoenzyme that accounts for this activity remains controversial. Methodology/Principal Findings In this study we present two related patients harbouring a novel PYGM mutation, p.R771PfsX33. In the patients skeletal muscle biopsies, PYGM mRNA levels were ∼60% lower than those observed in two matched healthy controls; biochemical analysis of a patient muscle biopsy resulted in undetectable GP protein and GP activity. A strong reduction of the PYGM mRNA was observed in cultured muscle cells from patients and controls, as compared to the levels observed in muscle tissue. In cultured cells, PYGM mRNA levels
|jats:p|The binding to glycogen phosphorylase b of glucose 6-phosphate and inorganic phosphate (respectively allosteric inhibitor and substrate/activator of the enzyme) were studied in the crystal at 0.3 nm (3A) resolution. Glucose 6-phosphate binds in the alpha-configuration at a site that is close to the AMP allosteric effector site at the subunit-subunit interface and promotes several conformational changes. The phosphate-binding site of the enzyme for glucose 6-phosphate involves contacts to two cationic residues, Arg-309 and Lys-247. This site is also occupied in the inorganic-phosphate-binding studies and is therefore identified as a high-affinity phosphate-binding site. It is distinct from the weaker phosphate-binding site of the enzyme for AMP, which is 0.27 nm (2.7A) away. The glucose moiety of glucose 6-phosphate and the adenosine moiety of AMP do not overlap. The results provide a structural explanation for the kinetic observations that glucose 6-phosphate inhibition of AMP activation of
OBJECTIVE--To determine whether transient ST-T alterations in patients with unstable angina are associated with an increase in plasma glycogen phosphorylase BB concentrations on admission to hospital. DESIGN--Prospective screening of patients with unstable angina for markers of myocardial cell damage. SETTING--Accident and emergency department of university hospital. PATIENTS--48 consecutive patients admitted for angina pectoris (18 with transient ST-T alterations). None of the patients had acute myocardial infarction according to standard criteria. MAIN OUTCOME MEASURES--Creatine kinase and creatine kinase MB activities, creatine kinase MB mass concentration, and myoglobin, cardiac troponin T, and glycogen phosphorylase BB concentrations on admission. RESULTS--All variables except for creatine kinase and creatine kinase MB activities were significantly higher on admission in patients with unstable angina and transient ST-T alterations than in patients without. However, glycogen phosphorylase BB ...
1LWN: Crystal structure of rabbit muscle glycogen phosphorylase a in complex with a potential hypoglycaemic drug at 2.0 A resolution
TY - JOUR. T1 - Intron/exon structure of the human gene for the muscle isozyme of glycogen phosphorylase. AU - Burke, J.. AU - Hwang, P.. AU - Anderson, L.. AU - Lebo, R.. AU - Gorin, Fredric A. AU - Fletterick, R.. PY - 1987. Y1 - 1987. N2 - The intron/exon organization of the human gene for glycogen phosphorylase has been determined. The segments of the polypeptide chain that corresponds to the 19 exons of the gene are examined for relationships between the three-dimensional structure to the protein and gene structure. Only weak correlations are observed between domains of phosphorylase and exons. The nucleotide binding domains that are found in phosphorylase and other glycolytic enzymes are examined for relationships between exons of the genes and structures of the domains. When mapped to the three-dimensional structures, the intron/exon boundaries are shown to be widely distributed in this family of protein domains.. AB - The intron/exon organization of the human gene for glycogen ...
Glycogen phosphorylase (GP) is a validated target for the development of new type 2 diabetes treatments. Exploiting the Zinc docking database, we report the in silico screening of 1888 N-acyl-beta-D-glucopyranosylamines putative GP inhibitors differing only in their R groups. CombiGlide and GOLD docking programs with different scoring functions were employed with the best performing methods combined in a consensus scoring approach to ranking of ligand binding affinities for the active site. Six selected candidates from the screening were then synthesized and their inhibitory potency was assessed both in vitro and ex vivo. Their inhibition constants values, in vitro, ranged from 5 to 377 mu M while two of them were effective at causing inactivation of GP in rat hepatocytes at low mu M concentrations. The crystal structures of GP in complex with the inhibitors were defined and provided the structural basis for their inhibitory potency and data for further structure based design of more potent ...
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Phosphorylase b is a non-active form and is present in resting muscle. Phosphorylase b kinase activity increases significantly when the Mg2+:ATP ratio exceeds. The breakd
1ABB: CONTROL OF PHOSPHORYLASE B CONFORMATION BY A MODIFIED COFACTOR: CRYSTALLOGRAPHIC STUDIES ON R-STATE GLYCOGEN PHOSPHORYLASE RECONSTITUTED WITH PYRIDOXAL 5-DIPHOSPHATE
Stimulation of hepatocytes with vasopressin (10 nM) in the presence of 1.25 mM extracellular Ca2+ increased glycogen phosphorylase activity 4-fold within 15s and provoked a rapid efflux of cell-associated Ca2+. Vasopressin also caused a transient increase in the Ca content of a mitochondria-rich fraction separated within seconds of hormone stimulation by a rapid fractionation technique [Shears & Kirk (1984) Biochem. J. 219, 375-382]. The Ca content of this fraction was restored to the control value within 2 min of hormone addition. These results indicate that mitochondria are not the source of the cell-associated Ca which is mobilized in the cytosol of vasopressin-stimulated hepatocytes. Rather, these organelles buffer the increase in cytosol [Ca2+] attributable to Ca mobilization from non-mitochondrial sources. ...
Rabbit Polyclonal Anti-Glycogen Phosphorylase BB/GPBB Antibody. Validated: WB, IHC, IHC-P. Tested Reactivity: Human, Mouse, Rat, and more. 100% Guaranteed.
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Looking for McArdle's syndrome? Find out information about McArdle's syndrome. A hereditary metabolic disorder caused by deficiency of muscle phosphorylase, with abnormal glycogen deposition in skeletal muscle leading to muscle fiber... Explanation of McArdle's syndrome
TY - JOUR. T1 - Phosphorylation of glycogen synthase by phosphorylase kinase. Stoichiometry, specificity and site of phosphorylation. AU - Soderling, Thomas. AU - Sheorain, Virender S.. AU - Ericsson, Lowell H.. PY - 1979/10/1. Y1 - 1979/10/1. UR - http://www.scopus.com/inward/record.url?scp=0018533336&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0018533336&partnerID=8YFLogxK. U2 - 10.1016/0014-5793(79)80723-1. DO - 10.1016/0014-5793(79)80723-1. M3 - Article. C2 - 115711. AN - SCOPUS:0018533336. VL - 106. SP - 181. EP - 184. JO - FEBS Letters. JF - FEBS Letters. SN - 0014-5793. IS - 1. ER - ...
SWISS-MODEL Template Library (SMTL) entry for 1pyg.1. STRUCTURAL BASIS FOR THE ACTIVATION OF GLYCOGEN PHOSPHORYLASE B BY ADENOSINE MONOPHOSPHATE
Stravodimos, G.A., Kantsadi, A.L., Apostolou, A., Kyriakis, E., Kafaski-Kanelli, V.N., Solovou, T.G.A., Gatzona, P., Liggri, P.C., Theofanous, S., Gorgogietas, V.A., Kissa, A., Psachoula, C., Chatzileontiadou, D.S.M., Lemonakis, A., Psarra, A.G., Skamnaki, V.T., Haroutounian, S., Leonidas, D.D. 2017. Affinity crystallography reveals the bioactive compounds of industrial juicing byproducts of Punica granatum for glycogen phosphorylase. Curr Drug Discov Technol. doi: 10.2174/1570163814666170619091736. [Epub ahead of print ...
Supplementary Materials Fig. on granzyme B and Compact disc107a manifestation by T cells. (a) Percentage of T cells that indicated granzyme B before and after activation in the cSCC and non\cSCC individuals. (b) Percentage of T cells that indicated CD107a before and after activation in the cSCC and non\cSCC individuals. Fig. S5. Gating strategy for… Continue reading Supplementary Materials Fig. ...
The present invention relates to substituted arylsulphonylglycines of general formula (I) wherein R, X, Y and Z are defined as in claim 1, the tautomers, enantiomers, diastereomers, mixtures thereof and salts thereof, which have valuable pharmacological properties, particularly the suppression of the interaction of glycogen phosphorylase a with the GL subunit of glycogen-associated protein phosphatase 1 (PP1), and their use as pharmaceutical compositions. ##STR00001##
SWISS-MODEL Template Library (SMTL) entry for 1gfz.1. FLAVOPIRIDOL INHIBITS GLYCOGEN PHOSPHORYLASE BY BINDING AT THE INHIBITOR SITE
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InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
Created after (Sernee et al., Cell Host & Microbe, 2019), in press [PMID=31513773]. The dual activity mannosyltransferases/phosphorylases of six Leishmania proteins allows the management of mannogen (storage polysacharride). Family evolutionary related the bacterial GH130 phosphorylases ...
pep:known chromosome:VEGA66:X:102513975:102644246:-1 gene:OTTMUSG00000018059 transcript:OTTMUST00000043585 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Phka1 description:phosphorylase kinase alpha 1 ...
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Glycogen phosphorylase isoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. This isoform of the enzyme exists in cardiac (heart) and brain tissue. The enzyme is one of the new cardiac markers which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. Other enzymes related to glycogen phosphorylase are abbreviated as GPLL (liver) and GPMM (muscle). Apple FS, Wu AH, Mair J, et al. (May 2005). Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome. Clin. Chem. 51 (5): 810-24. doi:10.1373/clinchem.2004.046292. PMID 15774573. Peetz D, Post F, Schinzel H, et al. (2005). Glycogen phosphorylase BB in acute coronary syndromes. Clin. Chem. Lab. Med. 43 (12): 1351-8. doi:10.1515/CCLM.2005.231. PMID 16309372 ...
Accepted name: phosphorylase kinase. Reaction: 2 ATP + phosphorylase b = 2 ADP + phosphorylase a. Other name(s): dephosphophosphorylase kinase; glycogen phosphorylase kinase; PHK; phosphorylase b kinase; phosphorylase B kinase; phosphorylase kinase (phosphorylating); STK17. Systematic name: ATP:phosphorylase-b phosphotransferase. Comments: Requires Ca2+ and calmodulin for activity. The enzyme phosphorylates a specific serine residue in each of the subunits of the dimeric phosphorylase b. For muscle phosphorylase but not liver phosphorylase, this is accompanied by a further dimerization to form a tetrameric phosphorylase. The enzyme couples muscle contraction with energy production via glycogenolysis glycolysis by catalysing the Ca2+-dependent phosphorylation and activation of glycogen phosphorylase b [5]. The γ subunit of the tetrameric αβγδ enzyme is the catalytic subunit.. Links to other databases: BRENDA, EXPASY, KEGG, Metacyc, PDB, CAS registry number: 9001-88-1. References:. 1. Krebs, ...
1. The properties of phosphorylase a, phosphorylase b, phosphorylase kinase and phosphorylase phosphatase present in a human haemolysate were investigated. The two forms of phosphorylase have the same affinity for glucose 1-phosphate but greatly differ in Vmax. Phosphorylase b is only partially stimulated by AMP, since, in the presence of the nucleotide, it is about tenfold less active than phosphorylase a. In a fresh human haemolysate phosphorylase is mostly in the b form; it is converted into phosphorylase a by incubation at 20degreesC, and this reaction is stimulated by glycogen and cyclic AMP. Once activated, the enzyme can be inactivated after filtration of the haemolysate on Sephadex G-25. This inactivation is stimulated by caffeine and glucose and inhibited by AMP and fluoride. The phosphorylase kinase present in the haemolysate can also be measured by the rate of activation of added muscle phosphorylase b, on addition of ATP and Mg2+. 2. The activity of phosphorylase kinase was measured ...
We examined the insulin dose-response characteristics of human muscle glycogen synthase and phosphorylase activation. We also determined whether increasing the rate of glucose disposal by hyperglycemia at a fixed insulin concentration activates glycogen synthase. Physiological increments in plasma insulin but not glucose increased the fractional activity of glycogen synthase. The ED50: s for insulin stimulation of whole body and forearm glucose disposal were similar and unaffected by glycemia. Glycogen synthase activation was exponentially related to the insulin-mediated component of whole body and forearm glucose disposal at each glucose concentration. Neither insulin nor glucose changed glycogen phosphorylase activity. These results suggest that insulin but not the rate of glucose disposal per se regulates glycogen synthesis by a mechanism that involves dephosphorylation of glycogen synthase but not phosphorylase. This implies that the low glycogen synthase activities found in ...
TY - JOUR. T1 - Epinephrine regulation of skeletal muscle glycogen metabolism. Studies utilizing the perfused rat hindlimb preparation. AU - Dietz, M. R.. AU - Chiasson, J. L.. AU - Soderling, T. R.. AU - Exton, J. H.. PY - 1980/12/1. Y1 - 1980/12/1. N2 - Studies of rat skeletal muscle glycogen metabolism carried out in a perfused hindlimb system indicated that epinephrine activates phosphorylase via the cascade of phosphorylation reactions classically linked to the β-adrenergic receptor/adenylate cyclase system. The β blocker propranolol completely blocked the effects of epinephrine on cAMP, cAMP-dependent protein kinase, phosphorylase, and glucose-6-P, whereas the α blocker phentolamine was totally ineffective. Omission of glucose from the perfusion medium did not modify the effects of epinephrine. Glycogen synthase activity in control perfused and nonperfused muscle was largely glucose-6-P-dependent (-glucose-6-P/+glucose-6-P activity ratios of 0.1 and 0.2, respectively). Epinephrine ...
Catalytic subunit of the phosphorylase b kinase (PHK), which mediates the neural and hormonal regulation of glycogen breakdown (glycogenolysis) by phosphorylating and thereby activating glycogen phosphorylase. In vitro, phosphorylates PYGM, TNNI3, MAPT/TAU, GAP43 and NRGN/RC3 (By similarity).
HEADER TRANSFERASE 25-AUG-05 2ATI TITLE GLYCOGEN PHOSPHORYLASE INHIBITORS COMPND MOL_ID: 1; COMPND 2 MOLECULE: GLYCOGEN PHOSPHORYLASE, LIVER FORM; COMPND 3 CHAIN: A, B; COMPND 4 SYNONYM: LIVER GLYCOGEN PHOSPHORYLASE A; COMPND 5 EC: 2.4.1.1; COMPND 6 ENGINEERED: YES SOURCE MOL_ID: 1; SOURCE 2 ORGANISM_SCIENTIFIC: HOMO SAPIENS; SOURCE 3 ORGANISM_COMMON: HUMAN; SOURCE 4 ORGANISM_TAXID: 9606; SOURCE 5 EXPRESSION_SYSTEM: SPODOPTERA FRUGIPERDA; SOURCE 6 EXPRESSION_SYSTEM_COMMON: FALL ARMYWORM; SOURCE 7 EXPRESSION_SYSTEM_TAXID: 7108 KEYWDS GLYCOGEN PHOSPHORYLASE, TRANSFERASE EXPDTA X-RAY DIFFRACTION AUTHOR T.KLABUNDE,K.U.WENDT,D.KADEREIT,V.BRACHVOGEL,H.J.BURGER,A.W.HERLING, AUTHOR 2 N.G.OIKONOMAKOS,D.SCHMOLL,E.SARUBBI,E.VON ROEDERN,K.SCHOENAFINGER, AUTHOR 3 E.DEFOSSA REVDAT 3 13-JUL-11 2ATI 1 VERSN REVDAT 2 24-FEB-09 2ATI 1 VERSN REVDAT 1 25-AUG-06 2ATI 0 JRNL AUTH T.KLABUNDE,K.U.WENDT,D.KADEREIT,V.BRACHVOGEL,H.J.BURGER, JRNL AUTH 2 A.W.HERLING,N.G.OIKONOMAKOS,M.N.KOSMOPOULOU,D.SCHMOLL, JRNL AUTH 3 ...
Isoproterenol (0.01-10 nM) caused the rapid, complete conversion of glycogen phosphorylase from the b to the a form in cultured C-6 astrocytoma cells. This was associated with a 60-fold elevation in cellular cyclic 3,5-AMP content. Both effects were blocked stereoselectively by (-)-propranolol. The beta adrenoceptor partial agonists (±)-salbutamol (1 nM-10 µM) and (±)-hydroxybenzylpindolol (0.1 nM-10 µM) also caused full conversion of phosphorylase b to a, although their maximal effects on cellular cyclic AMP content were only 80% and 17.5%, respectively, of that obtainable with (-)-isoproterenol. Prostaglandin E1 (PGE1), which caused only a 1.6-fold elevation in cyclic AMP content, gave rise to 54% conversion of phosphorylase b to the a form. Prior incubation of cells with 3-isobutyl-1-methylxanthine caused a 1.4-fold elevation of cyclic AMP and converted 36% of phosphorylase b to the a form. Under those conditions dibutyryl cyclic AMP fully activated phosphorylase b to a , and the ...
Looking for glycogen synthetase? Find out information about glycogen synthetase. An enzyme that catalyzes the synthesis of the amylose chain of glycogen Explanation of glycogen synthetase
The sequence of events set in motion through the activation of adenyl cyclase by E is: increase in cyclic 3,5-AMP → activation of phosphorylase b kinase → increase in phosphorylase a → increase in glycogen breakdown. Since cyclic 3,5-AMP is destroyed by a phosphodiesterase, its actual level in the tissues will depend on the relative rates of two opposing reactions, catalyzed by cyclase and diesterase (1, 20). Posner et al. (16) have shown that the concentration of cyclic 3,5-AMP increases in frog muscle after E administration. Concentrations of the order of 1 x 10-7 to 1 x 10-6 M activate the phosphorylase b kinase of muscle both in vivo and in vitro (10, 16). Phosphofructokinase, on the other hand, is activated in vitro by concentrations of cyclic 3,5-AMP so much higher than are present in muscle that one wonders whether this activation is of physiological importance (13). In the isolated frog sartorius incubated at 20°C in 5 x 10-7 M E a rise in phosphorylase a can be ...
BACKGROUND Phosphorylase kinase (PhK), also known as adenosine triphosphate (ATP)-phosphorylase b phosphotransferase, integrates multiple calcium/calmodulin-dependent signalling pathways, including those involved in cell migration and cell proliferation, while coupling these pathways to glycogenolysis and ATP-dependent phosphorylation, thus ensuring continuing energy supply for these activities. OBJECTIVES Our laboratory recently reported correlation of elevated PhK activity with psoriatic activity. This study further evaluates the significance of drug-induced suppression of PhK activity on psoriatic activity. PATIENTS AND METHODS PhK activity was assayed in four groups, each with 10 patients: (i) active untreated psoriasis; (ii) resolving psoriasis treated by calcipotriol (Dovonex(R), Bristol Myers Squibb, Princeton, NJ, U.S.A. ), a vitamin D3 analogue and an indirect inhibitor of PhK; (iii) curcumin (diferuloylmethane), a selective PhK inhibitor; and (iv) 10 normal non-psoriatic subjects.
To examine insulins acute action on gluconeogenic flux to G6P in the absence of its effects on glycogenolytic flux, we inhibited glycogen breakdown using a glycogen phosphorylase inhibitor. The drug used in these studies, BAY R3401, was previously shown to effectively suppress glycogenolysis in hepatocytes (11), in perfused intact liver (11), and in the whole animal (rat and dog) (12-14). The active metabolite of BAY R3401 reduces glycogenolysis both by facilitating inactivation of the enzyme through allosteric inhibition and by dephosphorylation of glycogen phosphorylase a (11). In the dog, after administration of BAY R3401, inhibition of NHGLY resulted in a decrease in hepatic glucose production and net hepatic lactate balance (NHLB) but had no effect on the metabolism (level or NHB) of other gluconeogenic precursors, NEFAs, pancreatic or adrenal hormones, or hepatic blood flow (14). Whereas glucose Ra decreased 50%, glucose Rd and clearance were unaffected, indicating that the portion of the ...
TY - JOUR. T1 - An essential function for the phosphate-dependent exoribonucleases RNase PH and polynucleotide phosphorylase. AU - Zhou, Zhihua. AU - Deutscher, Murray P.. PY - 1997/7. Y1 - 1997/7. N2 - Escherichia coli cells lacking both polynucleotide phosphorylase (PNPase) and RNase PH, the only known P1-dependent exoribonucleases, were previously shown to grow slowly at 37°C and to display a dramatically reduced level of tRNA(Tryrsu3+) suppressor activity. Here we show that the RNase PH-negative, PNP-negative double-mutant strain actually displays a reversible cold-sensitive phenotype and that tRNA biosynthesis is normal. In contrast, ribosome structure and function are severely affected, particularly at lower temperatures. At 31°C, the amount of 50S subunit is dramatically reduced and 23S rRNA is degraded. Moreover, cells that had been incubated at 42°C immediately cease growing and synthesizing protein upon a shift to 31°C, suggesting that the ribosomes synthesized at the higher ...
noun an inherited disease in which abnormal amounts of glycogen accumulate in skeletal muscle; results in weakness and cramping • Hypernyms: ↑genetic disease, ↑genetic disorder, ↑genetic abnormality, ↑genetic defect, ↑congenital disease,…
Numerous biomedical advances have been made since Carl and Gerty Cori discovered the enzyme phosphorylase in the 1940s and the Scottish physician Brian McArdle reported in 1951 a previously undescribed disorder characterized by a gross failure of the breakdown in muscle of glycogen. Today we know that this disorder, commonly known as McArdle disease, is caused by inherited deficiency of the muscle isoform of glycogen phosphorylase (GP). Here we review the main aspects of the pathogenomics of this disease including, among others: the spectrum of mutations in the gene (PYGM) encoding muscle GP; the interplay between the different tissue GP isoforms in cellular cultures and in patients; what can we learn from naturally occurring and recently laboratory-generated animal models of the disease; and potential therapies ...
We investigate the influence of insulin, glucagon and epinephrine on the core metabolism of hepatocytes by means of a kinetic model. These hormones induce significant alterations in certain metabolic activities of key enzymes like Glycogen synthase and Glycogen phosphorylase. Insulin is the primary anabolic hormone promoting the storage of energy by stimulating, for example, the glycogen synthesis. The effect of Glucagon and epinephrine are opposite that of insulin. They cause the liver to convert ...
Combining 2-Deoxy-D-glucose with fenofibrate leads to tumor cell death mediated by simultaneous induction of energy and ER stress. Huaping Liu, Metin Kurtoglu, Clara Lucia León-Annicchiarico, Cristina Munoz-Pinedo, Julio Barredo, Guy Leclerc, Jaime Merchan, Xiongfei Liu, Theodore J. Lampidis. 2016 May 10. [Epub ahead of print]. View Article. Targeting cisplatin-resistant human tumor cells with metabolic inhibitors. Sullivan EJ, Kurtoglu M, Brenneman R, Liu H, Lampidis TJ. Cancer Chemother Pharmacol. 2013 Dec 19. [Epub ahead of print]. View Article. Increased sensitivity to glucose starvation correlates with downregulation of glycogen phosphorylase isoform PYGB in tumor cell lines resistant to 2-deoxy-D-glucose. Philips KB, Kurtoglu M, Leung HJ, Liu H, Gao N, Lehrman MA, Murray TG, Lampidis TJ. Cancer Chemother Pharmacol. 2013 Dec 1. [Epub ahead of print]. View Article. Conversion of 2-deoxyglucose-induced growth inhibition to cell death in normoxic tumor cells. Liu H, Kurtoglu M, Cao Y, Xi H, ...
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Principal Investigator:AKIYAMA Shinichi, Project Period (FY):1998 - 1999, Research Category:Grant-in-Aid for Scientific Research (B), Section:一般, Research Field:Pathological medical chemistry
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A neuromuscular condition, it causes victims to experience fatigue and pain after only minimal exercise. It is caused by a genetic defect that results in a deficiency of a muscle enzyme.
PHKG1 - PHKG1 (untagged)-Kinase deficient mutant (K49M) of Human phosphorylase kinase, gamma 1 (muscle) (PHKG1) available for purchase from OriGene - Your Gene Company.
Hi al, Am looking for sources for the following antibodies to be used for human paraffin embedded tissues: THYMIDINE PHOSPHORYLASE THYYMIDYLATE SYNTHASE CTYDINE DEAMINASE DIHYDROPRYIMDINE DEHYDROGENASE any info will be greatly appreciated ...
Family created after Kuhaudomlarp et al. J. Biol. Chem. (2018) [PMID=29317507] who have shown that the Euglena gracilis enzyme is a b-1,3-glucan phosphorylase. Distant sequence similarities suggest this family forms clan GH-Q with family GH94 ...
Recombinant protein of human thymidine phosphorylase (TYMP), transcript variant 2, 20 ug available for purchase from OriGene - Your Gene Company.