Aminoimidazole Carboxamide: An imidazole derivative which is a metabolite of the antineoplastic agents BIC and DIC. By itself, or as the ribonucleotide, it is used as a condensation agent in the preparation of nucleosides and nucleotides. Compounded with orotic acid, it is used to treat liver diseases.Glutamate Formimidoyltransferase: A PYRIDOXAL PHOSPHATE-containing enzyme that catalyzes the transfer of a formyl group from L-GLUTAMATE to N-formimidoyl-L-glutamate and TETRAHYDROFOLATE. This enzyme may also catalyze formyl transfer from 5-formyltetrahydrofolate to L-GLUTAMATE. This enzyme was formerly categorized as EC 2.1.2.6.Phosphoribosylaminoimidazolecarboxamide Formyltransferase: An enzyme that catalyzes the conversion of aminoimidazole-4-carboxamide ribonucleotide to 5-formyl-aminoimidazole-4-carboxamide ribonucleotide in the purine de novo synthesis pathway. It requires the cofactor N(10)-FORMYLTETRAHYDROFOLATE as the formyl donor.Hydroxymethyl and Formyl Transferases: Enzymes that catalyze the transfer of hydroxymethyl or formyl groups. EC 2.1.2.Ribonucleotides: Nucleotides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)Carbon-Nitrogen Ligases: Enzymes that catalyze the joining of two molecules by the formation of a carbon-nitrogen bond. EC 6.3.Phosphoribosylglycinamide Formyltransferase: An enzyme that catalyzes the transfer of a formyl group from N10-formyltetrahydrofolate to N1-(5-phospho-D-ribosyl)glycinamide to yield N2-formyl-N1-(5-phospho-D-ribosyl)glycinamide and tetrahydrofolate. It plays a role in the de novo purine biosynthetic pathway.Thiamine: 3-((4-Amino-2-methyl-5-pyrimidinyl)methyl)-5-(2- hydroxyethyl)-4-methylthiazolium chloride.Carbon-Nitrogen Ligases with Glutamine as Amide-N-Donor: Enzymes that catalyze the joining of glutamine-derived ammonia and another molecule. The linkage is in the form of a carbon-nitrogen bond. EC 6.3.5.Agelas: A genus of large, brightly colored SPONGES in the family Agelasidae, possessing a skeleton of spongin fibers with a core of large spicules (megascleres).Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Carboxy-Lyases: Enzymes that catalyze the addition of a carboxyl group to a compound (carboxylases) or the removal of a carboxyl group from a compound (decarboxylases). EC 4.1.1.Ligases: A class of enzymes that catalyze the formation of a bond between two substrate molecules, coupled with the hydrolysis of a pyrophosphate bond in ATP or a similar energy donor. (Dorland, 28th ed) EC 6.Salmonella enterica: A subgenus of Salmonella containing several medically important serotypes. The habitat for the majority of strains is warm-blooded animals.Ribonucleosides: Nucleosides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)Nucleotide Deaminases: Catalyze the hydrolysis of nucleotides with the elimination of ammonia.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

Absorption, metabolism, and excretion of 14C-temozolomide following oral administration to patients with advanced cancer. (1/623)

The purpose of this study is to characterize the absorption, metabolism, and excretion of carbon 14-labeled temozolomide (14C-TMZ) administered p.o. to adult patients with advanced solid malignancies. On day 1 of cycle 1, six patients received a single oral 200-mg dose of 14C-TMZ (70.2 microCi). Whole blood, plasma, urine, and feces were collected from days 1-8 and on day 14 of cycle 1. Total radioactivity was measured in all samples. TMZ, 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC), and 4-amino-5-imidazole-carboxamide (AIC) concentrations were determined in plasma, and urine and plasma samples were profiled for metabolite/degradation products. Maximum TMZ plasma concentrations were achieved between 0.33 to 2 h (mean, 1.2 h), and half-life, apparent volume of distribution, and oral clearance values averaged 1.9 h, 17 liters/m2, and 104 ml/min/m2, respectively. A first-order absorption, one-compartment linear model, which included first-order formation of MTIC from TMZ and elimination of MTIC via degradation to AIC, and a peripheral distribution compartment for AIC, adequately described the plasma TMZ, MTIC, and AIC concentrations. MTIC systemic clearance was estimated to be 5384 ml/min/m2, and the half-life was calculated to be 2.5 min. Metabolite profiles of plasma at 1 and 4 h after treatment showed that 14C-derived radioactivity was primarily associated with TMZ, and a smaller amount was attributed to AIC. Profiles of urine samples from 0-24 h revealed that 14C-TMZ-derived urinary radioactivity was primarily associated with unchanged drug (5.6%), AIC (12%), or 3-methyl-2,3-dihydro-4-oxoimidazo[5,1-d]tetrazine-8-carboxyl ic acid (2.3%). The recovered radioactive dose (39%) was principally eliminated in the urine (38%), and a small amount (0.8%) was excreted in the feces. TMZ exhibits rapid oral absorption and high systemic availability. The primary elimination pathway for TMZ is by pH-dependent degradation to MTIC and further degradation to AIC. Incomplete recovery of radioactivity may be explained by the incorporation of AIC into nucleic acids.  (+info)

Apoptosis induced by growth factor withdrawal in fibroblasts overproducing fructose 2,6-bisphosphate. (2/623)

Fructose 2,6-bisphosphate is a potent endogenous stimulator of glycolysis. A high aerobic glycolytic rate often correlates with increased cell proliferation. To investigate this relationship, we have produced clonal cell lines of Rat-1 fibroblasts that stably express transgenes coding for 6-phosphofructo-2-kinase, which catalyzes the synthesis of fructose 2,6-bisphosphate, or for fructose 2,6-bisphosphatase, which catalyzes its degradation. While serum deprivation in culture reduced the growth rate of control cells, it caused apoptosis in cells overproducing fructose 2,6-bisphosphate. Apoptosis was inhibited by 5-amino-4-imidazolecarboxamide riboside, suggesting that 5'-AMP-activated protein kinase interferes with this phenomenon.  (+info)

Effect of AMPK activation on muscle glucose metabolism in conscious rats. (3/623)

The effect of AMP-activated protein kinase (AMPK) activation on skeletal muscle glucose metabolism was examined in awake rats by infusing them with 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR; 40 mg/kg bolus and 7.5 mg. kg-1. min-1 constant infusion) along with a variable infusion of glucose (49.1 +/- 2.4 micromol. kg-1. min-1) to maintain euglycemia. Activation of AMPK by AICAR caused 2-deoxy-D-[1,2-3H]glucose (2-DG) uptake to increase more than twofold in the soleus and the lateral and medial gastrocnemius compared with saline infusion and occurred without phosphatidylinositol 3-kinase activation. Glucose uptake was also assessed in vitro by use of the epitrochlearis muscle incubated either with AICAR (0.5 mM) or insulin (20 mU/ml) or both in the presence or absence of wortmannin (1.0 microM). AICAR and insulin increased muscle 2-DG uptake rates by approximately 2- and 2.7-fold, respectively, compared with basal rates. Combining AICAR and insulin led to a fully additive effect on muscle glucose transport activity. Wortmannin inhibited insulin-stimulated glucose uptake. However, neither wortmannin nor 8-(p-sulfophenyl)-theophylline (10 microM), an adenosine receptor antagonist, inhibited the AICAR-induced activation of glucose uptake. Electrical stimulation led to an about threefold increase in glucose uptake over basal rates, whereas no additive effect was found when AICAR and contractions were combined. In conclusion, the activation of AMPK by AICAR increases skeletal muscle glucose transport activity both in vivo and in vitro. This cellular pathway may play an important role in exercise-induced increase in glucose transport activity.  (+info)

5' AMP-activated protein kinase activation causes GLUT4 translocation in skeletal muscle. (4/623)

It has previously been reported that exercise causes an increase in glucose uptake in skeletal muscle and also an increase in 5' AMP-activated protein kinase (AMPK) activity. 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICA-riboside), an analog of adenosine, is taken up into cells and phosphorylated to form AICA-riboside monophosphate (ZMP), which can also activate AMPK. This study was designed to determine whether the increase in glucose uptake observed with AMPK activation by AICA-riboside is due to GLUT4 translocation from an intracellular location to the plasma membranes, similar to that seen in response to contraction. Rat hindlimbs were perfused with Krebs-Henseleit bicarbonate containing 4% bovine serum albumin, washed bovine erythrocytes, 8 mmol/l glucose, and +/-2 mmol/AICA-riboside or +/-60 nmol/l insulin. Perfusion medium containing AICA-riboside was found to significantly increase AMPK activity, glucose uptake, and GLUT4 translocation in skeletal muscle above basal levels. Insulin-perfused muscles showed significant increases in glucose uptake and GLUT4 translocation, but AMPK activation was not significantly changed from basal levels. These results provide evidence that the increased glucose uptake observed with AMPK activation by AICA-riboside in perfused rat hindlimb muscles is due to an increase in the translocation of GLUT4 to surface membranes.  (+info)

Translocation of myocardial GLUT-4 and increased glucose uptake through activation of AMPK by AICAR. (5/623)

Insulin increases glucose uptake through the translocation of GLUT-4 via a pathway mediated by phosphatidylinositol 3-kinase (PI3K). In contrast, myocardial glucose uptake during ischemia and hypoxia is stimulated by the translocation of GLUT-4 to the surface of cardiac myocytes through a PI3K-independent pathway that has not been characterized. AMP-activated protein kinase (AMPK) activity is also increased by myocardial ischemia, and we examined whether AMPK stimulates glucose uptake and GLUT-4 translocation. In isolated rat ventricular papillary muscles, 5-aminoimidazole-4-carboxyamide-1-beta-D-ribofuranoside (AICAR), an activator of AMPK, as well as cyanide-induced chemical hypoxia and insulin, increased 2-[(3)H]deoxyglucose uptake two- to threefold. Wortmannin, a PI3K inhibitor, did not affect either the AICAR- or the cyanide-stimulated increase in deoxyglucose uptake but eliminated the insulin-stimulated increase in deoxyglucose uptake. Immunofluorescence studies demonstrated translocation of GLUT-4 to the myocyte sarcolemma in response to stimulation with AICAR, cyanide, or insulin. Preincubation of papillary muscles with the kinase inhibitor iodotubercidin or adenine 9-beta-D-arabinofuranoside (araA), a precursor of araATP (a competitive inhibitor of AMPK), decreased AICAR- and cyanide-stimulated glucose uptake but did not affect basal or insulin-stimulated glucose uptake. In vivo infusion of AICAR caused myocardial AMPK activation and GLUT-4 translocation in the rat. We conclude that AMPK activation increases cardiac muscle glucose uptake through translocation of GLUT-4 via a pathway that is independent of PI3K. These findings suggest that AMPK activation may be important in ischemia-induced translocation of GLUT-4 in the heart.  (+info)

Improvement by 5-amino-4-imidazole carboxamide riboside of the contractile dysfunction that follows brief periods of ischemia through increases in ecto-5-nucleotidase activity and adenosine release in canine hearts. (6/623)

5-Amino-4-imidazole carboxamide (AICA) riboside increases adenosine release in ischemic myocardium, suggesting that AICA riboside improves contractile dysfunction. In 49 open-chest dogs, contractile function assessed by fractional shortening (FS) was observed 3 h after the onset of reperfusion following 15 min of occlusion of the left anterior descending coronary artery. During reperfusion, the treatment with AICA riboside increased adenosine concentration in the coronary venous blood (536+/-44 vs. 281+/-21 pmol/ml at 3 min of reperfusion, p<0.001) and peak coronary hyperemic flow (367+/-13 vs. 300+/-21 ml/100 g per min, p<0.001) when compared with the untreated group. FS at 3h of reperfusion increased in the AICA riboside group (21.1+/-2.3 vs. 12.8+/-0.6% in the untreated group, p<0.001). AICA riboside increased myocardial ecto-5'-nucleotidase activity. Administration of adenosine also augmented coronary hyperemic flow and increased FS to the levels of the AICA riboside group. Either 8-phenyltheophylline (an antagonist of adenosine receptors) or alpha,beta-methylene-adenosine 5'-diphosphate (an inhibitor of ecto-5'-nucleotidase) completely abolished the increased coronary hyperemic flow and improvements of myocardial contractile function due to AICA riboside. Thus it was concluded that AICA riboside improves the contractile dysfunction that follows a brief period of ischemia via adenosine-dependent mechanisms.  (+info)

Effect of methotrexate on blood purine and pyrimidine levels in patients with rheumatoid arthritis. (7/623)

OBJECTIVE: The mechanism of anti-inflammatory effects of methotrexate (MTX) at low dose may relate to a decrease in availability of the purine precursor or it may depend on accumulation of 5-aminoimidazole-4-carboxamide (AICAR) and the anti-inflammatory nucleoside adenosine. The aim of this study was to evaluate the possible mechanism of action by analysis of changes in blood concentrations of purine and pyrimidine metabolites during MTX treatment. METHODS: Venous blood samples were collected from rheumatoid arthritis patients before and at different times for up to 7 days after the start of MTX treatment. Whole blood concentrations of adenosine, uridine, hypoxanthine, uric acid and erythrocyte nucleotides were measured by HPLC. RESULTS: The initial blood adenosine concentration was 0.073 +/- 0.013 microM and no differences were observed during MTX treatment. However, a decrease in uric acid concentration was observed from 205.5+/-13.5 to 160. 9+/-13.5 microM (P<0.05) within 24 h after MTX administration. The hypoxanthine concentration decreased in parallel with uric acid, while the uridine concentration decreased 48 h after MTX administration. No accumulation of AICAR-triphosphate (ZTP) was observed in the erythrocytes. CONCLUSIONS: MTX decreases circulating purine and pyrimidine concentrations, and their availability for DNA and RNA synthesis, which may affect immune cell proliferation and protein (cytokine) expression. The absence of adenosine concentration changes and lack of ZTP formation is evidence against an AICAR/adenosine mechanism, although localized adenosine concentration changes cannot be excluded.  (+info)

Chronic activation of 5'-AMP-activated protein kinase increases GLUT-4, hexokinase, and glycogen in muscle. (8/623)

This study was designed to determine whether chronic chemical activation of AMP-activated protein kinase (AMPK) would increase glucose transporter GLUT-4 and hexokinase in muscles similarly to periodic elevation of AMPK that accompanies endurance exercise training. The adenosine analog, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), has previously been shown to be taken up by cells and phosphorylated to form a compound (5-aminoimidazole-4-carboxamide ribonucleotide) that mimics the effect of AMP on AMPK. A single injection of AICAR resulted in a marked increase in AMPK in epitrochlearis and gastrocnemius/plantaris muscles 60 min later. When rats were injected with AICAR (1 mg/g body wt) for 5 days in succession and were killed 1 day after the last injection, GLUT-4 was increased by 100% in epitrochlearis muscle and by 60% in gastrocnemius muscle in response to AICAR. Hexokinase was also increased approximately 2. 5-fold in the gastrocnemius/plantaris. Gastrocnemius glycogen content was twofold higher in AICAR-treated rats than in controls. Chronic chemical activation of AMPK, therefore, results in increases in GLUT-4 protein, hexokinase activity, and glycogen, similarly to those induced by endurance training.  (+info)

*Inosine monophosphate synthase

It has two functions: EC 2.1.2.3 - 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase EC 3.5.4.10 - IMP ... Vergis JM, Bulock KG, Fleming KG, Beardsley GP (2001). "Human 5-aminoimidazole-4-carboxamide ribonucleotide transformylase/ ... "Entrez Gene: ATIC 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase". Rasmussen HH, van Damme ... 2004). "Polyglutamation of methotrexate with common polymorphisms in reduced folate carrier, aminoimidazole carboxamide ...

*Chemotherapy

It primarily inhibits the enzyme thymidylate synthase, but also has effects on DHFR, aminoimidazole carboxamide ribonucleotide ...

*Acadesine

... (INN), also known as 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside, AICA-riboside, and AICAR, is an AMP- ... Cronstein, BN; Kamen, BA (2007). "5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICA-riboside) as a targeting agent ... Corton JM, Gillespie JG, Hawley SA, Hardie DG (April 1995). "5-aminoimidazole-4-carboxamide ribonucleoside. A specific method ... "5-Aminoimidazole-4-Carboxamide 1- -D-Ribofuranoside Acutely Stimulates Skeletal Muscle 2-Deoxyglucose Uptake in Healthy Men". ...

*AICA ribonucleotide

5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) is an intermediate in the generation of inosine monophosphate. AICAR is ... 5-aminoimidazole-4-carboxamide ribonucleoside. A specific method for activating AMP-activated protein kinase in intact cells? ... 5-Aminoimidazole-4-carboxamide-1- β - d -ribofuranoside Increases Myocardial Glucose Uptake during Reperfusion and Induces Late ... 2006)doi:10.1152/ajpheart.00906.2005 Longnus SL, Wambolt RB, Parsons HL, Brownsey RW, Allard MF 5-Aminoimidazole-4-carboxamide ...

*List of MeSH codes (D03)

... aminoimidazole carboxamide MeSH D03.383.129.308.040 --- antazoline MeSH D03.383.129.308.080 --- biotin MeSH D03.383.129.308.090 ...

*Adenylosuccinate lyase deficiency

... both of which involve the β-elimination of fumarate to produce aminoimidazole carboxamide ribotide (AICAR) from SAICAR or ...

*Phosphoribosylaminoimidazolecarboxamide formyltransferase

The systematic name of this enzyme class is 10-formyltetrahydrofolate:5-phosphoribosyl-5-amino-4-imidazole-carb oxamide N- ... aminoimidazolecarboxamide ribonucleotide transformylase, and transformylase. As of late 2007, 11 structures have been solved ...

*Reduced folate carrier family

... reduced folate carrier-mediated folate/antifolate transport through an antiport mechanism with 5-aminoimidazole-4-carboxamide ...

*Adenylosuccinate lyase

... to 5-aminoimidazole-4-carboxamide ribotide (AICAR) and fumarate. AICAR proceeds through three more reactions before it becomes ... In the first reaction, ASL converts 5-aminoimidazole- (N-succinylocarboxamide) ribotide (SAICAR) ...

*Biosynthesis

... forming N-succinyl-5-aminoimidazole-4-carboxamide ribonucleotide (SAICAR). SAICAR lyase removes the carbon skeleton of the ... leaving the amino group and forming 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR). AICAR transformylase transfers a ... Firestine, SM; Poon, SW; Mueller, EJ; Stubbe, J; Davisson, VJ (Oct 4, 1994). "Reactions catalyzed by 5-aminoimidazole ... forming the 5-membered imidazole ring 5-aminoimidazole ribonucleotide (AIR). N5-CAIR synthetase transfers a carboxyl group, ...

*Ribonucleotide

... the removal of the carbon skeleton of aspartate by SAICAR lyase results in 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR ... as 5-aminoimidazole ribonucleotide (AIR). A carboxyl group is attached to AIR by N5-CAIR synthetase to form N5- ... along with amino group from aspartate forms an amide bond to create N-succinyl-5-aminoimidazale-4-carboxamide ribonucleotide ( ... forming N-formylaminoimidazole-4-carboxamide ribonucleotide (FAICAR). Lastly, closure of the second ring structure is carried ...

*Ribavirin

... and replacement with an amino group results in the natural purine synthetic precursor 5-aminoimidazole-4-carboxamide-1-β-D- ... Ribavirin's carboxamide group can make the native nucleoside drug resemble adenosine or guanosine, depending on its rotation. ... The most successful ribavirin derivative to date is the 3-carboxamidine derivative of the parent 3-carboxamide, first reported ... 4-triazole-3-carboxamide". Science. 177 (4050): 705-6. doi:10.1126/science.177.4050.705. PMID 4340949. Smith RA & Kirkpatrick W ...

*Proline oxidase

Activation of AMP-activated protein kinase (AMPK), the cellular energy sensor, by 5-aminoimidazole-4-carboxamide ribonucleoside ...

*Formylation

In the penultimate step of de novo purine biosynthesis, 5-aminoimidazole-4-carboxyamide ribotide (AICAR) is formylated to 5- ... formaminoimidazole-4-carboxamide ribotide (FAICAR)by AICAR transformylase. PurN GAR transformylase is found in eukaryotes and ... These reactions are catalyzed by the enzymes glycinamide ribonucleotide (GAR) transformylase and 5-aminoimidazole-4- ...
The present study shows for the first time that (1) AMPK activation by AICAR directly causes vasodilation of skeletal muscle resistance arteries by enhancing NO production in endothelium and (2) acute AICAR-induced stimulation of AMPK in vivo enhances microvascular perfusion in skeletal muscle. This is the first report of such an effect, which suggests a role for AMPK in the vasodilation responsible for increased microvascular perfusion, the purpose of which is to increase available capillary surface area for increased nutrient and hormone delivery to skeletal muscle myocytes. We found that AICAR activated AMPK in endothelium and, to a minor extent, in smooth muscle cells of muscle resistance arteries and relaxes these arteries by increasing NO synthesis. Thus, AICAR-induced AMPK activation and endothelial NO production is the most likely mechanism underlying AICAR-stimulated microvascular perfusion in muscle in vivo.. Our results strongly suggest that AICARs vasodilator effects in muscle ...
BACKGROUND: Insulin-induced microvascular recruitment is important for optimal muscle glucose uptake. 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR, an activator of AMP-activated protein kinase), can also induce microvascular recruitment, at doses that do not acutely activate glucose transport in rat muscle. Whether low doses of AICAR can augment physiologic insulin action is unknown. In the present study we used the euglycemic hyperinsulinemic clamp to assess whether insulin action is augmented by low dose AICAR. METHODS: Anesthetized rats were studied during saline infusion or euglycemic insulin (3 mU/kg/min) clamp for 2 h in the absence or presence of AICAR for the last hour (5 mg bolus followed by 3.75 mg/kg/min). Muscle glucose uptake (Rg) was determined radioisotopically with (14)C-2-deoxyglucose and muscle microvascular perfusion by contrast-enhanced ultrasound with microbubbles. RESULTS: AICAR did not affect blood glucose, or lower leg Rg, although it significantly (p | 0.05)
The Rab-GTPase-activating proteins TBC1D1 and TBC1D4 (AS160) were previously shown to regulate GLUT4 translocation in response to activation of AKT and AMP-dependent kinase. However, knockout mice lacking either Tbc1d1 or Tbc1d4 displayed only partially impaired insulin-stimulated glucose uptake in fat and muscle tissue. The aim of this study was to determine the impact of the combined inactivation of Tbc1d1 and Tbc1d4 on glucose metabolism in double-deficient (D1/4KO) mice. D1/4KO mice displayed normal fasting glucose concentrations but had reduced tolerance to intraperitoneally administered glucose, insulin, and AICAR. D1/4KO mice showed reduced respiratory quotient, indicating increased use of lipids as fuel. These mice also consistently showed elevated fatty acid oxidation in isolated skeletal muscle, whereas insulin-stimulated glucose uptake in muscle and adipose cells was almost completely abolished. In skeletal muscle and white adipose tissue, the abundance of GLUT4 protein, but not GLUT4 ...
Imidazole Carboxamide (Dacarbazine) chemotherapy side effects, how its given, how it works, precautions and self care tips for treatment of multiple cancers
It is frequently assumed that increased capacity for lipid catabolism and increased activity of fatty acid oxidation result inevitably in increased energy expenditure and reduction of body fat stores. In fact, this simplified view has motivated in part the whole AMPK research. However, as it was also stressed recently by Cooney and colleagues (Hoehn et al. 2010), thermodynamically, the only way to decrease body fat in the absence of changes in physical activity is to decrease the efficiency of energy conversion or to decrease food intake (Hoehn et al. 2010). Accordingly, stimulation of whole-body lipid oxidation in mice either in response to activation of AMPK following 10-day-lasting AICAR treatment or to genetic disruption of acetyl-CoA carboxylase 2 gene had no effect on adiposity (Hoehn et al. 2010). That prolonged treatment of mice by the AMPK activator AICAR resulted in reduction of adiposity (Giri et al. 2006) could perhaps be explained by a stimulation of energy expenditure linked to ...
No hope of ever seeing this in bulk is there? Its outrageously expensive in small amounts now. AMP-kinase activation with AICAR simultaneously
Effects of an AICAR treatment on the differentiation of MC3T3-E1 cells. AICAR (0.5 mM), a AMP kinase stimulator, was added after the cells reached confluency. T
Ultraviolet (UV) radiation and reactive oxygen species (ROS) impair the physiological functions of retinal pigment epithelium (RPE) cells by inducing cell apoptosis, which is the main cause of age-related macular degeneration (AMD). The mechanism by which UV/ROS induces RPE cell death is not fully addressed. Here, we observed the activation of a ceramide-endoplasmic reticulum (ER) stress-AMP activated protein kinase (AMPK) signaling axis in UV and hydrogen peroxide (H2O2)-treated RPE cells. UV and H2O2 induced an early ceramide production, profound ER stress and AMPK activation. Pharmacological inhibitors against ER stress (salubrinal), ceramide production (fumonisin B1) and AMPK activation (compound C) suppressed UV- and H2O2-induced RPE cell apoptosis. Conversely, cell permeable short-chain C6 ceramide and AMPK activator AICAR (5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide) mimicked UV and H2O2s effects and promoted RPE cell apoptosis. Together, these results suggest that UV/H2O2 activates the
Our results show that, even in LKB1-null tumor cells, activation of AMPK is sufficient for cell-cycle arrest, and necessary for the arrest induced by Ca2+-elevating agents. Inhibition of cell proliferation and G1 arrest in response to AMPK activation has been demonstrated previously in cells expressing LKB1 (12-14). However, those studies relied on the use of the pharmacologic activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), which can have AMP-independent "off-target" effects (42), or on overexpression of activated AMPK, which might also lead to nonphysiologic effects. Our results show that the G1 arrest (25) and consequent inhibition of proliferation (24) caused by the reexpression of LKB1 in LKB1-null tumor cells is mediated by AMPK and not by any of the AMPK-related kinases (ARK). We have previously shown that the ARKs that have detectable activity in HeLa cells, that is, SIK1, SIK2, SIK3, NUAK2, MARK1, MARK2/3, and MARK4, were (unlike AMPK) not activated in the cells by ...
Attention! In the May issue of Drug Testing and Analysis (Thevis. 2011), Mario Thevis and his colleagues from the Center for Preventive Doping Research - Institute of Biochemistry at the German Sport University in Cologne report that the powdered form of AICAR they had purchased from dubious Internet sources along with GW1516 another AMPK agonist and PPARδ modulator and a SARM (MK-2866), back in 2010, and which had passed customs mislabeled as containing amino acids and green tea extract did in fact contain the inosine monophosphate intermediate 5-Aminoimidazole-4-carboxamide ribotide. Yet, of the 100mg of white powder the scientists received, only 45% contained the active ingredient. In this context it is also noteworthy, that a) AICAR is not yet approved as a drug by any federal agency, I know of, so that your doctor could not even prescribe it at the moment and b) it is not even likely that it will ever be approved, because BigPharma wont be interested in a naturally occurring and thus ...
Product Number , 74454497. CAS Number , 72-40-2. EC , 200-778-3. Molecular Formula , C4H6N4OHCl. Molecular Weight , 162.58. Storage Temp , Harmonized Tariff code , 29332990. Signal Word , ...
Creative-Proteomics offer cas 6974-32-9 1-O-acetyl 2, 3, 5-tri-O-benzoyl-β-D-[UL-13C5] ribofuranoside. We are specialized in manufacturing Stabel Isotope Labeled Analytical Standard products.
Background: 17-β-estradiol has been shown to play an important role in regulating vascular function and vasomotor tone. We have previously demonstrated sex differences in rapid estrogen receptor signaling during vascular relaxation. We recently observed that estrogen activates AMPK-activated protein kinase (AMPK), suggesting that AMPK is a likely mediator of estrogen receptor (ER) signaling in vasomotor function. AMPK has been reported to participate in vascular relaxation. Furthermore, our recent studies found that incubating vascular rings with 5-aminoimidazole-4-carboxamide (AICAR), an AMPK activator, results in greater vasorelaxation of female C57BL/6J mouse vessels when compared with male vessels. However, the precise mechanisms involving estrogen receptor signaling and AMPK in promoting vascular relaxation remain unknown.. Methods and Results: To elucidate a critical role of ERα-AMPK signaling and downstream targets involved in vascular relaxation, including the potential sex difference ...
Effects of siRNA-AdipoR1 transfection or AICAR treatments on Osterix mRNA expression in MC3T3-E1 cells. Total RNA was collected at 4, 7, 10 days after siRNA-Adi
Searching for some dosing information for the AICAR in the Ripped to the Bone Stack on Research Peptides.. http://www.precisionpeptides.com/store/Stacks/Ripped%20to%20the%20Bone%20Stack.html I am good with everything else, but I am not too familiar with this and cannot find anything on it, or I am not looking in the right place. This will be my first Peptide Cycle also.. If this is a better option, please weigh in..
Structure, properties, spectra, suppliers and links for: N-(2-Ethyl-6-methylphenyl)-2,3-dimethyl-4H-thieno[3,2-c]thiopyran-6-carboxamide.
Buy high quality (5α,17β)-N-Methoxy-N-methyl-3-oxo-4-azaandrost-1-ene-17-carboxamide 138689-15-3 from toronto research chemicals Inc.
Suppliers List, E-mail/RFQ Form, Molecular Structure, Weight, Formula, IUPAC, Synonyms for (2r)-n-(2,6-dimethylphenyl)-1-propylpiperidine-2-carboxamide (CAS No. 98717-16-9)
The 5′ adenosine monophosphate-activated protein kinase (AMPK) is a heterotrimeric, evolutionary conserved enzyme which has emerged as a critical regulator of skeletal muscle cellular bioenergetics. AMPK is activated by both chemical (adipokines) and mechanical (stretch, contraction) stimuli leading to metabolic changes within muscle cells that include increased fatty acid oxidation, glucose uptake and glycolysis, as well as the stimulation and regulation of mitochondrial biogenesis. Collectively these acute responses and chronic adaptations act to reduce cellular disturbances, resulting in tighter metabolic control and maintenance of energy homeostasis. This brief review will describe the structure, function and activation of AMPK in skeletal muscle and how this ubiquitous molecule may be a plausible target for the treatment of several lifestyle-related metabolic disorders.
It has previously been reported that exercise causes an increase in glucose uptake in skeletal muscle and also an increase in 5 AMP-activated protein kinase (AMPK) activity. 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICA-riboside), an analog of adenosine, is taken up into cells and phosphorylated to form AICA-riboside monophosphate (ZMP), which can also activate AMPK. This study was designed to determine whether the increase in glucose uptake observed with AMPK activation by AICA-riboside is due to GLUT4 translocation from an intracellular location to the plasma membranes, similar to that seen in response to contraction. Rat hindlimbs were perfused with Krebs-Henseleit bicarbonate containing 4% bovine serum albumin, washed bovine erythrocytes, 8 mmol/l glucose, and +/-2 mmol/AICA-riboside or +/-60 nmol/l insulin. Perfusion medium containing AICA-riboside was found to significantly increase AMPK activity, glucose uptake, and GLUT4 translocation in skeletal muscle above basal ...
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Exercise-induced glucose uptake in skeletal muscle is mediated by an insulin-independent mechanism, but the actual signals to glucose transport in response to muscle contraction have not been identified. The 5´-AMP-activated protein kinase (AMPK) has emerged as a putative mediator of contraction-induced glucose transport, although no conclusive evidence has been provided so far. Recent experiments in AMPK transgenic mice suggest that glucose transport induced by 5-amino-4-imidazolecarboxamide riboside (AICAR) or hypoxia is mediated by AMPK. In contrast, contraction-induced glucose transport in rodent skeletal muscle induced by electrical stimulation in vitro or in situ is not influenced or is only partially reduced by abolishing both or one of the catalytic AMPK subunits. This is compatible with exercise studies done in humans, where no tight correlation is found between AMPK activity and glucose uptake during exercise. Taken together, these results question an essential role of AMPK in ...
The AMP-activated protein kinase (AMPK) is a metabolic stress-sensing αβγ heterotrimer responsible for energy homeostasis. Pharmacological inhibition of AMPK is regarded as a therapeutic strategy in some disease settings including obesity and cancer; however, the broadly used direct AMPK inhibitor compound C suffers from poor selectivity. We have discovered a dihydroxyquinoline drug (MT47-100) with novel AMPK regulatory properties, being simultaneously a direct activator and inhibitor of AMPK complexes containing the β1 or β2 isoform, respectively. Allosteric inhibition by MT47-100 was dependent on the β2 carbohydrate-binding module (CBM) and determined by three non-conserved CBM residues (Ile81, Phe91, Ile92), but was independent of β2-Ser108 phosphorylation. Whereas MT47-100 regulation of total cellular AMPK activity was determined by β1/β2 expression ratio, MT47-100 augmented glucose-stimulated insulin secretion from isolated mouse pancreatic islets via a β2-dependent mechanism. Our
Mammalian AMP-activated protein kinase presents strong structural and functional similarities with the yeast sucrose non-fermenting 1 (Snf1) kinase involved in the derepression of glucose-repressed genes. It is now clearly established that AMP-activated protein kinase in the liver decreases glycolytic/lipogenic gene expression as well as genes involved in hepatic glucose production. This is achieved through a decreased transcriptional efficiency of transcription factors such as sterol-regulatory-element-binding protein-1c, carbohydrate-response-element-binding protein, hepatocyte nuclear factor 4α or forkhead-related protein. Clearly, the long-term consequences of AMP-activated protein kinase activation have to be taken into account if activators of this enzyme are to be designed as anti-diabetic drugs.. ...
Autophagy is a process by which eukaryotic cells engulf and break down cellular components to provide new substrates for metabolism. Egan et al. (see the Perspective by Hardie) report a biochemical mechanism by which low energy stores in a cell can be linked to autophagy. The authors searched for targets of the adenosine monophosphate-activated protein kinase (AMPK), which is activated when cellular concentrations of adenosine triphosphate are depleted. AMPK was found to regulate another protein kinase, ULK1, which functions in regulation of autophagy. Cells engineered so that ULK1 could not be phosphorylated by AMPK failed to respond properly to starvation, had decreased autophagy, and were prone to starvation-induced cell death.. D. F. Egan, D. B. Shackelford, M. M. Mihaylova, S. Gelino, R. A. Kohnz, W. Mair, D. S. Vasquez, A. Joshi, D. M. Gwinn, R. Taylor, J. M. Asara, J. Fitzpatrick, A. Dillin, B. Viollet, M. Kundu, M. Hansen, R. J. Shaw, Phosphorylation of ULK1 (hATG1) by AMP-activated ...
If you have problems with a majority of the weight loss pillars, you might consider increasing the activity of a key cellular switch: AMPK (adenosine monophosphate-activated protein kinase). AMPK is… ...
AMPK (5′-AMP-activated protein kinase) is emerging as a metabolic master switch, by which cells in both mammals and lower organisms sense and decode changes in energy status. Changes in AMPK activity have been shown to regulate glucose transport in muscle and glucose production by the liver. Moreover, AMPK appears to be a key regulator of at least one transcription factor linked to a monogenic form of diabetes mellitus. As a result, considerable efforts are now under way to explore the usefulness of AMPK as a therapeutic target for other forms of this disease. Here we review this topic, and discuss new findings which suggest that AMPK may play roles in regulating insulin release and the survival of pancreatic islet β-cells, and nutrient sensing by the brain.. ...
Objective- Vascular endothelial cells (ECs) confer atheroprotection at locations of the arterial tree where pulsatile laminar flow (PS) exists with a high shear stress and a large net forward direction. We investigated whether the PS-induced expression of the transcription factor Krüppel-Like Factor 2 (KLF2) in cultured ECs and its expression in the mouse aorta is regulated by AMP-activated protein kinase (AMPK).. Methods and Results- AMPK inhibition by Compound C or siRNA had a significant blocking effect on the PS-induced KLF2 expression. The induction of KLF2 by PS led to the increase in eNOS and the suppression of ET-1, which could be reversed by KLF2 siRNA. In addition, PS induced the phosphorylation of ERK5 and MEF2 which are necessary for the KLF2 expression. These mechanotransduction events were abrogated by the blockade of AMPK. Furthermore, the phosphorylation levels of ERK5 and MEF2, as well as the expression of KLF2, were significantly reduced in the aorta of AMPKα2 knockout mice ...
Identification of phosphorylation sites in AMP-activated protein kinase (AMPK) for upstream AMPK kinases and study of their roles by site-directed ...
AMP-activated protein kinase (AMPK) is an evolutionally conserved protein kinase that serves as an energy guardian to help cells adapt to various metabolic stress including hypoxia. Because the role of AMPK in cancers has not been fully elucidated, in this study we investigated the expression and activation of AMPK in lung adenocarcinoma (LADC) cells and tissue ...
AMP-activated protein kinase (AMPK) plays diverse roles and coordinates complex metabolic pathways for maintenance of energy homeostasis. This could be explained by the fact that AMPK exists as multiple heterotrimer complexes comprising a catalytic α subunit (α1, α2) and regulatory β (β1, β2) and γ (γ1, γ2, γ3) subunits, which are uniquely distributed across different cell types. There has been keen interest in developing specific and isoform-selective AMPK-activating drugs for therapeutic use and also as research tools. Moreover, establishing ways of enhancing cellular AMPK activity would be beneficial for both purposes. Here, we investigated if a recently-described potent AMPK-activator called 991, in combination with a commonly used activator AICAR or contraction, further enhances AMPK activity and glucose transport in mouse skeletal muscle ex vivo. Given that γ3 is exclusively expressed in skeletal muscle and is implicated in contraction-induced glucose transport, we measured the ...
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Role of AMPK2 in basal, training-, and AICAR-induced GLUT4, hexokinase II, and mitochondrial protein expression in mouse muscle Am J Physiol Endocrinol Metab 292: E331-E339, 2007. First published September 5, 2006; doi:10.1152/ajpendo.00243.2006.- We investigated the role of AMPK2 in basal, exercise training-, and AICAR-induced protein expression of GLUT4, hexokinase II (HKII), mitochondrial markers, and AMPK…
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Connexios Life Sciences and Boehringer Ingelheim are collaborating on the development of AMP-activated protein kinase (AMPK) stimulants for the treatment of
Author: Bitrián Satorra, M.; Genre: Thesis; Published online: 2011; Title: Regulation of plant stress responses by AMP-activated protein kinases
Of interest were the observations that after cells had accumulated ZMP, and AICAR was removed or 5-iodotubercidin was added, the intracellular ZMP level rapidly decreased and the augmentation of folate transport was reversed. Hence, continued synthesis of ZMP is required to sustain intracellular ZMP levels and the augmentation of RFC-mediated transport. Neither AICAR itself nor ZTP within the cells resulted in augmentation of folate transport. The basis for the rapid decrease of intracellular ZMP under these conditions is due in part to the conversion of ZMP to ZTP and to export mediated by RFC. It is also possible that a component of the decrease in cell ZMP was due to rapid hydrolysis back to the base.. This interaction between ZMP and folates at the level of a common carrier is a classic exchange reaction in which the transmembrane gradient for one substrate drives the uphill transport of another. Most uphill systems for members of the SLC superfamily of solute transport carriers derive their ...
AMPK alpha 1 + AMPK alpha 2小鼠单克隆抗体[34.2](ab80039)可与小鼠, 大鼠, 人, 果蝇样本反应并经WB, IP, ELISA, IHC, ICC/IF实验严格验证,被4篇文献引用并得到5个独立的用户反馈。
Abstract AMP-activated protein kinase (AMPK) is a stress signaling enzyme that orchestrates the regulation of energy-generating and -consuming pathways. Intrinsic AMPK activation p..
0001 Vynález sa týka zlúčenin, ktoré sú priamymi aktivátormi AMPK (AMPaktivovanej proteínkinázy) a ich použitia pri liečení porúch regulovaných deaktiváciou AMPK. Napríklad zlúčeniny podľa vynálezu sú použiteľné naDoterajší stav techniky a úvod vynálezu0002 AMPK je dobre zavedený ako senzor a regulátor homeostázy bunkovej energie (Hardie D. G. a Hawley S. A., AMP-activated protein kinase the energy charge hypothesis revisited Bioassays, 23, 1112, (2001), Kemp B. E. a kol. AMP-activated protein kinase, super metabolic regulator, Biochem Soc. Transactions, 31. 162 (2003. Alosterická aktivácia tejto kinázy vdaka zvýšeniu množstva AMP vedie k stavom svyčerpaním bunkovej energie. Výsledná fosforylácia serínu/treoninu cieľových enzýmov vedie kadaptácii bunkového metabolizmu na nízkoenergetický stav. Celkový efekt zmien vyvolaných aktiváciou AMPK je inhibícia procesov spotrebovávajúcich ATP a aktivácia metabolických ciest vytvárajúcich ATP, a ...
Buy Bupivacaine impurity B (2RS)-N-(2,6-dimethylphenyl)piperidine-2-carboxamide - CAS Number 65797-42-4 from LGC Standards. Please login or register to view prices, check availability and place orders.
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In cancer cells, the epithelial-mesenchymal transition (EMT) confers the ability to invade basement membranes and metastasize to distant sites, establishing it as an appealing target for therapeutic intervention. Here, we report a novel function of the master metabolic kinase AMPK in suppressing EMT by modulating the Akt-MDM2-Foxo3 signaling axis. This mechanistic link was supported by the effects of siRNA-mediated knockdown and pharmacological activation of AMPK on epithelial and mesenchymal markers in established breast and prostate cancer cells. Exposure of cells to OSU-53, a novel allosteric AMPK activator, as well as metformin and AICAR, was sufficient to reverse their mesenchymal phenotype. These effects were abrogated by AMPK silencing. Phenotypic changes were mediated by Foxo3a activation, insofar as silencing or overexpressing Foxo3a mimicked the effects of AMPK silencing or OSU-53 treatment on EMT, respectively. Mechanistically, Foxo3a activation led to the transactivation of the ...
AMP-activated protein kinase (AMPK) functions as a sensor to maintain energy balance and is therefore a potential target for drug design against metabolic syndrome. The crystal structure of the complex between the phosphorylated-state mimic T172D mutant AMPK α2 kinase domain and a selective inhibitor, compound C, has been determined, revealing the unique inhibitor-binding mode of this protein kinase ...
AMPK alpha 2山羊多克隆抗体(ab105028)可与小鼠, 大鼠, 人样本反应并经WB, sELISA实验严格验证。所有产品均提供质保服务,中国75%以上现货。
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The ratio between ATP and AMP is used as a way for a cell to sense how much energy is available and control the metabolic pathways that produce and consume ATP. The body attempts to maintain a specific ratio of AMP:ATP; when this ratio is out of balance, the cells adjust their metabolism accordingly. As the ratio increases either by increased levels of AMP or decreased levels of ATP, the body is signaled to produced more ATP. The AMP:ATP ratio is primarily regulated by an enzyme known as AMP-activated protein kinase (AMPK). When activated, AMPK sets in motion a series of events which switch cells from active ATP consumption to ATP production ...
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N-(2,6-DICHLOROPYRIDIN-3-YL)-1H-IMIDAZOLE-5-CARBOXAMIDE/ACM240815514 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and services.
During 2 years, we enrolled 25 patients diagnosed with typewriter tinnitus and evaluated the types of AICA loops in the IAC and CPA and the types of neurovascular contact by using 3T 3D T2-VISTA imaging in 15 patients. When we compared the symptomatic sides of patients with typewriter tinnitus (group 1) with the asymptomatic sides of those with typewriter tinnitus (group 2) and healthy controls (group 3), the difference was not statistically significant (Table). However, considering that in a previous study, type II and type III AICA loops were observed in 38.0% of 332 patients with ipsilateral auditory symptoms,13 our results, which demonstrated that 56.3% of group 1 and 18.8% of group 3 had type II and III AICA loops, showed a definite tendency toward type II and III AICA loops on the symptomatic sides of subjects with typewriter tinnitus. Moreover, the 3 groups in this study had significantly different (Table) neurovascular contact types. In group 1, 68.8% of the subjects showed type II or ...
Contraindicaciones del ampk. adversos, si bien la píldora del día después no presenta particulares indicaciones de uso, ni muchos efectos particulares,.
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Purpose: : AMP-activated protein kinase (AMPK) is a serine/threonine protein kinase, which senses cellular energy change, and helps regulate cellular metabolism. 5-Aminoimidazole-4-carboxamide riboside (AICAR) is taken up by cells, converted to ZMP (an analog of AMP) and is used as a pharmacologic activator of AMPK. It has recently been shown that AICAR can cause growth arrest in various cancer cell lines. We chose to investigate the effect and mechanism of action of AICAR on the growth of primary and metastatic uveal melanoma cell lines. Methods: : Growth Inhibition Assay: Primary and metastatic uveal melanoma cell lines were cultured in the presence of 1, 2 and 4mM AICAR for 3-5 days. In separate experiments, cells were pretreated with 0.1 uM Iodotubericin (inhibits conversion of AICAR to ZMP) or 2 uM dipyridamole (inhibits the entry of AICAR into the cells). At the end of the incubation, cell growth was assessed with the MTT assay. Flow cytometry for cell cyle analysis: Uveal melanoma cells ...
Half of the worlds population experiences Helicobacter pylori (H. pylori) infection, which is a main cause of gastritis, duodenal and gastric ulcer, and gastric cancers. In the current study, we investigated the potential role of compound 13 (C13), a novel α1-selective small molecule activator of AMP-activated protein kinase (AMPK), against H. pylori-induced cytotoxicity in cultured gastric epithelial cells (GECs). We found that C13 induced significant AMPK activation, evidenced by phosphorylation of AMPKα1 and ACC (acetyl-CoA carboxylase), in both primary and transformed GECs. Treatment of C13 inhibited H. pylori-induced GEC apoptosis. AMPK activation was required for C13-mediated GEC protection. Inhibition of AMPK kinase activity by the AMPK inhibitor Compound C, or silencing AMPKα1 expression by targeted-shRNAs, alleviated C13-induced GEC protective activities against H. pylori. Significantly, C13 inhibited H. pylori-induced reactive oxygen species (ROS) production in GECs. C13 induced ...
Hypoxic inhibition of K+ channels in type I cells is believed to be of central importance in carotid body chemotransduction. We have recently suggested that hypoxic channel inhibition is mediated by AMP-activated protein kinase (AMPK). Here, we have further explored the modulation by AMPK of recombinant K+ channels (expressed in HEK293 cells) whose native counterparts are considered O2-sensitive in the rat carotid body. Inhibition of maxiK channels by AMPK activation with AICAR was found to be independent of [Ca2+]i and occurred regardless of whether the α subunit was co-expressed with an auxiliary β subunit. All effects of AICAR were fully reversed by the AMPK inhibitor compound C. MaxiK channels were also inhibited by the novel AMPK activator A-769662 and by intracellular dialysis with the constitutively active, truncated AMPK mutant, T172D. The molecular identity of the O2-sensitive leak K+ conductance in rat type I cells remains unclear, but shares similarities with TASK-1 and TASK-3. Recombinant
Background & Aims: Aspirin reduces the incidence of and mortality from colorectal cancer (CRC) by unknown mechanisms. Cancer cells have defects in signaling via the mechanistic target of rapamycin (mTOR), which regulates proliferation. We investigated whether aspirin affects adenosine monophosphate-activated protein kinase (AMPK) and mTOR signaling in CRC cells. Methods: The effects of aspirin on mTOR signaling, the ribosomal protein S6, S6 kinase 1 (S6K1), and eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1) were examined in CRC cells by immunoblotting. Phosphorylation of AMPK was measured; the effects of loss of AMPKa on the aspirin-induced effects of mTOR were determined using small interfering RNA (siRNA) in CRC cells and in AMPK mouse embryonic fibroblasts. LC3 and ULK1 were used as markers of autophagy. We analyzed rectal mucosa samples from patients given 600 mg aspirin, once daily for 1 week. Results: Aspirin reduced mTOR signaling in CRC cells by inhibiting the ...
Activated AMPK promotes all the processes needed to maintain a youthful profile. However, AMPK activity fades with age. As previously mentioned, AMPK is activated in the presence of increased AMP. Therefore, to test the anti-aging properties of AMPK, researchers used fruit flies that were genetically engineered to synthesize higher levels of AMP. The research found that the modified flies lived up to one-third longer as a result of increased AMPK activity. "The life span benefit of these mutations depends upon increased AMP:ATP and ADP:ATP ratios and adenosine monophosphate-activated protein kinase (AMPK). Transgenic expression of AMPK in adult fat body or adult muscle, key metabolic tissues, extended life span" (Stenesen, 2013 ...
Abstract There are three isoforms of peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA, which promotes mitochondrial biogenesis in skeletal muscles. Compared with PGC-1α-a mRNA, PGC-1α-b or PGC-1α-c mRNA is transcribed by a different exon 1 of the PGC-1α gene. In this study, effects of exercise intensity and 5-aminoimidazole-4-carboxamide-1β-d-ribofuranoside (AICAR) on isoform-specific expressions of PGC-1α were…
Results HD feeding plus low-dose STZ injection successfully induced T2DM. Compared to normal control, diabetic mice manifested higher fasting-blood glucose level, lower glucose tolerance in OGTT examination (n=12, p,0.05), but there was no difference in plasma insulin levels. RSV alleviated MI/R injury in both normal and diabetic mice, as evidenced by decreased infarct size, cardiomyocytes apoptosis, caspase-3 activity, improved cardiac function (n=10, all p,0.05). Moreover, RSV treatment improved APN level, upregulated APN multimerisation both in plasma and adipose tissue, and increased DsbA-L expression in adipose tissue in diabetic mice (all p,0.01). Conversely, administration of AMPK inhibitor Compound C significantly attenuated the cardioprotective effects of RSV (all p,0.05).. ...
5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) is an intermediate in the generation of inosine monophosphate. AICAR is an analog of adenosine monophosphate (AMP) that is capable of stimulating AMP-dependent protein kinase (AMPK) activity. AICAR has been used clinically to treat and protect against cardiac ischemic injury. The drug was first used in the 1980s as a method to preserve blood flow to the heart during surgery. Currently, the drug has also been shown as a potential treatment for diabetes by increasing the metabolic activity of tissues by changing the physical composition of muscle. The nucleoside form of AICAR, acadesine, is an analog of adenosine that enters cardiac cells to inhibit adenosine kinase and adenosine deaminase. It enhances the rate of nucleotide re-synthesis increasing adenosine generation from adenosine monophosphate only during conditions of myocardial ischemia. In cardiac myocytes, acadesine is phosphorylated to AICAR to activate AMPK without changing the levels ...
We read with interest the article by Lai and coworkers1 published in Circulation about the favorable cardiovascular and metabolic effects of inorganic nitrite and metformin in patients with pulmonary hypertension in heart failure with preserved ejection fraction. Accumulating studies have demonstrated the therapeutic effects of stimulating the nitrate-nitrite-nitric oxide (NO) pathway in renal, cardiovascular, and metabolic disorders. However, the underlying mechanisms are still being debated.. Patients with metabolic syndrome are generally considered to have a higher risk of developing pulmonary hypertension in heart failure with preserved ejection fraction. In this study, Lai et al use a novel animal model of combined metabolic syndrome and pulmonary hypertension in heart failure with preserved ejection fraction and demonstrate that long-term treatment with inorganic nitrate combined with nitrite for 12 weeks reduces pulmonary pressures and vascular remodeling and improves glycemic control. ...
Integrins are cell surface receptors that physically bridge the extracellular matrix to the cytoskeleton and responsible for adhesion, migration, and signaling. Integrin function is intimately controlled by their membrane traffic. For example, integrins are dynamically internalized from the cell posterior and recycled to the cell anterior during cell migration. Misregulation of integrins is intimately linked with cancer progression, including metastasis and cell proliferation and survival. We have recently uncovered that integrin membrane traffic is controlled by AMP-activated protein kinase (AMPK), an energy stress sensing kinase within cells at becomes activated upon energy stress such as by an increase in cell AMP:ATP ratio. I confirmed that AMPK activation resulted in a reduction of cell surface β1-integrin. Using assays that selectively measure integrin exocytosis and endocytosis, I found that AMPK activation regulates β1-integrin recycling and possibly endocytosis. I demonstrated that ...
In the adult brain, programmed death of neural stem cells is considered to be critical for tissue homeostasis and cognitive function and is dysregulated in neurodegeneration. Previously, we have reported that adult rat hippocampal neural (HCN) stem cells undergo autophagic cell death (ACD) following insulin withdrawal. Because the apoptotic capability of the HCN cells was intact, our findings suggested activation of unique molecular mechanisms linking insulin withdrawal to ACD rather than apoptosis. Here, we report that phosphorylation of autophagy-associated protein p62 by AMP-activated protein kinase (AMPK) drives ACD and mitophagy in HCN cells. Pharmacological inhibition of AMPK or genetic ablation of the AMPK alpha 2 subunit by clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 genome editing suppressed ACD, whereas AMPK activation promoted ACD in insulin-deprived HCN cells. We found that following insulin withdrawal AMPK phosphorylated p62 at a novel site, ...
Recently, fatty acid transport across the plasma membrane has been shown to be a key process that contributes to the regulation of fatty acid metabolism in the heart. Since AMP kinase activation by 5-aminoimidazole-4-carboxamide-1-beta-D: -ribofurano
AICAR Powder Sarm Weight Loss Steroid Acadesine / Aicar For Bodybuilding Supplements Basic info. Product Name AICAR CAS 2627-69-2 Molecular Formula C9H14N4O5 Molecular Weight 258.231 Assay 99% Grade Pharmaceutical Grade Appearance White Crystalline...
AMP-activated protein kinase (AMPK) is an enzyme that senses and regulates cellular energy balance thus playing a key role in homeostasis. As such it is a target for treatment of metabolic disorders such as type II diabetes. AMPK is a hetero-trimeric complex composed of an α, β and γ subunit. α contains the catalytic kinase domain, β is a scaffolding subunit that enables complex formation and γ monitors cellular energy via nucleotide binding to its CBS domains. AMPK is primarily activated by phosphorylation at Thr-172 on the activation loop in the kinase domain. It exerts its cellular effects via phosphorylation of a range of downstream targets involved in different aspects of energy production & utilization. The aim of this thesis is to characterize the mechanistic basis of energy regulation of mammalian AMPK via structural and binding measurements. Fluorescence studies have been facilitated by the use of N-methylanthraniloyl (mant) labelled AMP and of β-Nicotinamide adenine dinucleotide ...
5AMP-activated protein kinase (AMPK) can be activated in response to cellular fuel depletion and leads to switching off ATP-consuming pathways and switching on ATP-regenerating pathways in many cell types. We have hypothesized that AMPK is a central mediator of insulin-independent glucose transport, which enables fuel-depleted muscle cells to take up glucose for ATP regeneration under conditions of metabolic stress. To test this hypothesis, rat epitrochlearis muscles were isolated and incubated in vitro under several conditions that evoke metabolic stress accompanied by intracellular fuel depletion. Rates of glucose transport in the isolated muscles were increased by all of these conditions, including contraction (5-fold above basal), hypoxia (8-fold), 2,4-dinotrophenol (11-fold), rotenone (7-fold), and hyperosmolarity (8-fold). All of these stimuli simultaneously increased both alpha1 and alpha2 isoform-specific AMPK activity. There was close correlation between alpha1 (r2 = 0.72) and alpha2 ...
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The 5′-adenosine monophosphate-activated serine/threonine protein kinase (AMPK) is stimulated by energy depletion, increase in cytosolic Ca2+ activity, oxidative stress, and nitric oxide. AMPK partici
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Sigma-Aldrich offers abstracts and full-text articles by [H T Kwan, David W Chan, Patty C H Cai, Celia S L Mak, Mingo M H Yung, Thomas H Y Leung, Oscar G W Wong, Annie N Y Cheung, Hextan Y S Ngan].
A new study describes how hyperactivation of AMP-activated protein kinase (AMPK) promotes neurodegeneration in Huntingtons disease (HD).
D942 compound: a furancarboxylic acid derivative, which increases glucose uptake in L6 myocytes through AMP-activated protein kinase (AMPK) activation
A common factor underlies various health-promoting diets: an enzyme called AMP-activated protein kinase. Many botanicals also activate this enzyme
According to ChemSpider.com, compound C12H22O11 is sucrose, also known as table sugar. Sugar is a sweetener used in numerous culinary applications. It is generally derived from either sugar beet or...
1. J Clin Invest. 2001 Oct;108(8):1167-74. Role of AMP-activated protein kinase in mechanism of metformin action. Zhou G, Myers R, Li Y, Chen Y, Shen X, Fenyk-Melody ...
3,5-diamino-N-(3-aminopropyl)-6-chloropyrazine-2-carboxamide: may be useful for thymine-related single nucleotide polymorphism detection; structure in first source
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184691-64-3 - QHVJCBYHXQLABN-UHFFFAOYSA-N - 1H-Pyrido(3,4-b)indole-6-carboxamide, 2,3,4,9-tetrahydro-N-(1,1-dimethyl-2-hydroxyethyl)-9-methyl-1-oxo- - Similar structures search, synonyms, formulas, resource links, and other chemical information.
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1H-Indole-7-carboxamide/ACM1670899 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and services.
Adenylosuccinase catalyses two reactions in purine metabolism: the conversion of succinylaminoimidazole carboxamide ribotide (SAICAR) into aminoimidazole carboxamide ribotide (AICAR) along the de novo synthesis of purine nucleotides, and the conversion of adenylosuccinate (S-AMP) into AMP in the conversion of IMP into AMP. The hallmarks of adenylosuccinase deficiency are the presence of succinylaminoimidazole carboxamide riboside (SAICAriboside) and succinyladenosine (S-Ado) in body fluids. These normally undetectable succinylpurines are the products of the dephosphorylation, by cytosolic 5-nucleotidase, of the two substrates of adenylosuccinase. The clinical picture of the enzyme deficiency is markedly heterogeneous with, as a rule, a profound, but nevertheless variable degree of psychomotor delay, often convulsions and/or autistic features, sometimes growth retardation and muscular dystrophy. The diagnostic tests that can be used for diagnosis, the enzyme and gene defects that have been ...
5-AMP-activated protein kinase (AMPK) has been suggested to be a metabolic master switch regulating various aspects of muscle glucose and fat metabolism. In isolated rat skeletal muscle, glucose suppresses the activity of AMPK and in human muscle glycogen loading decreases exercise-induced AMPK activation. We hypothesized that oral glucose ingestion during exercise would attenuate muscle AMPK activation. Nine male subjects performed two bouts of one-legged knee-extensor exercise at 60% of maximal workload. The subjects were randomly assigned to either consume a glucose containing drink or a placebo drink during the two trials. Muscle biopsies were taken from the vastus lateralis before and after 2 h of exercise. Plasma glucose was higher (6.0 +/- 0.2 vs. 4.9 +/- 0.1 mmol L-1, P , 0.001), whereas glycerol (44.8 +/- 7.8 vs. 165.7 +/- 22.3 micromol L-1), and free fatty acid (169.3 +/- 9.5 vs. 1161 +/- 144.9 micromol L-1) concentrations were lower during the glucose compared to the placebo trial ...
In this issue of the JCI, Zhou and coworkers provide evidence that the elusive target of metformins actions is the AMP-activated protein kinase (AMPK) (8). In studies performed in isolated hepatocytes and rat skeletal muscles, they demonstrate that metformin leads to AMPK activation, accompanied by an inhibition of lipogenesis (due to inactivation of acetyl-CoA carboxylase and suppression of lipogenic enzyme expression), suppression of the expression of SREBP-1 (a central lipogenic transcription factor), and a modest stimulation of skeletal muscle glucose uptake. Similar hepatic effects are seen in metformin-treated rats. Based on the use of a newly discovered AMPK inhibitor, their data suggest that the ability of metformin to suppress glucose production in hepatocytes requires AMPK activation. Many of these effects are similar to that of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a known, albeit nonspecific, activator of AMPK (9). However, metformin does not lead to AMPK activation ...
The kinase eEF2K [eukaryotic elongation factor 2 (eEF2) kinase] controls the rate of peptide chain elongation by phosphorylating eEF2, the protein that mediates the movement of the ribosome along the mRNA by promoting translocation of the transfer RNA from the A to the P site in the ribosome. eEF2K-mediated phosphorylation of eEF2 on threonine 56 (Thr56) decreases its affinity for the ribosome, thereby inhibiting elongation. Here, we show that in response to genotoxic stress, eEF2K was activated by AMPK (adenosine monophosphate-activated protein kinase)-mediated phosphorylation on serine 398. Activated eEF2K phosphorylated eEF2 and induced a temporary ribosomal slowdown at the stage of elongation. Subsequently, during DNA damage checkpoint silencing, a process required to allow cell cycle reentry, eEF2K was degraded by the ubiquitin-proteasome system through the ubiquitin ligase SCFβTrCP (Skp1-Cul1-F-box protein, β-transducin repeat-containing protein) to enable rapid resumption of translation ...
Arthritis and Rheumatism [00043591], 66(12), 3476-85. DOI:10.1002/art.38865. Funk, R. S., van Haandel, L. Becker, M. L., & Leeder, J. S. (2013). Low-dose Methotrexate Results in the Selective Accumulation of Aminoimidazole Carboxamide Ribotide in an Erythroblastoid Cell Line. J Pharm Exp Ther, 347, 154-63.. Kazmi, F. Hensley, T. Pope, C. Funk, R. S., Loewen, G. J., Buckley, D. B., & Parkinson, A. (2013). Lysosomal sequestration (trapping) of lipophilic amine (cationic amphiphilic) drugs in immortalized human hepatocytes (Fa2N-4 cells). Drug Metab Dispos, 41, 897-905.. Logan, R. Funk, R. S., Axcell, E. & Krise, J. P. (2012). Drug-drug interactions involving lysosomes: mechanisms and potential clinical implications. Expert Opinion on Drug Metabolism & Toxicology, 8, 943-58.. Funk, R. S., Brown, J. T., & Abdel-Rahman, S. M. (2012). Pediatric Pharmacokinetics: Human Development and Drug Disposition. Pediatr Clin North Am, 59, 1001-16.. Funk, R. S., & Krise, J. P. (2012). Cationic amphiphilic drugs ...
AMP/ATP-binding subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Gamma non-catalytic subunit mediates binding to AMP, ADP and ATP, leading to activate or inhibit AMPK: AMP-binding results in allosteric activation of alpha catalytic subunit (PRKAA1 or PRKAA2) both by inducing phosphorylation and preventing dephosphorylation of catalytic subunits. ADP also stimulates phosphorylation, without stimulating already ...
Abstract. Vincristine is extensively used chemotherapeutic medicine to treat leukemia. However, it remains a critical clinical problem with regard to its toxicity and drug-resistance. AMP-activated protein kinase (AMPK) is an energy sensor that is pivotal in maintaining cell metabolic homeostasis. It is reported that AMPK is involved in vincristine-induced apoptosis. However, whether AMPK is involved in chemotherapy-resistance is largely unclear. It is well-documented that metformin, a widely used medicine to treat type II diabetes, possesses anti-cancer activities, yet whether metformin affects leukemia cell viability via vincristine is unknown. In this study, we showed that both AMPKα1 mRNA and phosphorylated AMPK protein levels were significantly decreased in clinical leukemia samples. We further demonstrated that metformin sensitized leukemia cells to vincristine-induced apoptosis in an AMPK-dependent manner. In addition, knockdown of AMPKα1 significantly reduced the effects of metformin ...
Non-catalytic subunit of AMP-activated protein kinase (AMPK), an energy sensor protein kinase that plays a key role in regulating cellular energy metabolism. In response to reduction of intracellular ATP levels, AMPK activates energy-producing pathways and inhibits energy-consuming processes: inhibits protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. AMPK acts via direct phosphorylation of metabolic enzymes, and by longer-term effects via phosphorylation of transcription regulators. Also acts as a regulator of cellular polarity by remodeling the actin cytoskeleton; probably by indirectly activating myosin. Beta non-catalytic subunit acts as a scaffold on which the AMPK complex assembles, via its C-terminus that bridges alpha (PRKAA1 or PRKAA2) and gamma subunits (PRKAG1, PRKAG2 or PRKAG3) (By similarity).
Accurate methods needed to combat AICAR doping 5-Aminoimidazole-4-carboxamide-1--D-ribofuranoside AICAR or acadesine occurs naturally at low levels in the human body, but is also used as a performance-enhancing drug in sport. It is believed to increase endurance and was suspected to have been used in the 2009 Tour de France. AICAR has been banned...
Epidemiological studies have shown that infants exposed to an increased supply of nutrients before birth are at increased risk of type 2 diabetes in later life. We have investigated the hypothesis that fetal overnutrition results in reduced expression and phosphorylation of the cellular fuel sensor, AMP-activated kinase (AMPK) in liver and skeletal muscle before and after birth. From 115 days gestation, ewes were fed either at or 55% above maintenance energy requirements. Postmortem was performed on lamb fetuses at 139-141 days gestation (n = 14) and lambs at 30 days of postnatal age (n = 21), and liver and quadriceps muscle were collected at each time point. The expression of AMPK1 and AMPK2 mRNA was determined by quantitative RT-PCR (qRT-PCR). The abundance of AMPK and phospho-AMPK (P-AMPK) was determined by Western blot analysis, and the proportion of the total AMPK pool that was phosphorylated in each sample (%P-AMPK) was determined. The ratio of AMPK2 to AMPK1 mRNA expression was lower in ...
Heterotrimeric AMP-activated protein kinase (AMPK) is crucial for energy homeostasis of eukaryotic cells and organisms. Here we report on (i) bacterial expression of untagged mammalian AMPK isoform combinations, all containing gamma(1), (ii) an automated four-dimensional purification protocol, and (iii) biophysical characterization of AMPK heterotrimers by small angle x-ray scattering in solution (SAXS), transmission and scanning transmission electron microscopy (TEM, STEM), and mass spectrometry (MS). AMPK in solution at low concentrations (~1 mg/ml) largely consisted of individual heterotrimers in TEM analysis, revealed a precise 1:1:1 stoichiometry of the three subunits in MS, and behaved as an ideal solution in SAXS. At higher AMPK concentrations, SAXS revealed concentration-dependent, reversible dimerization of AMPK heterotrimers and formation of higher oligomers, also confirmed by STEM mass measurements. Single particle reconstruction and averaging by SAXS and TEM, respectively, revealed similar
5-AMP-activated protein kinase subunit beta-2 is an enzyme that in humans is encoded by the PRKAB2 gene. The protein encoded by this gene is a regulatory subunit of the AMP-activated protein kinase (AMPK). AMPK is a heterotrimer consisting of an alpha catalytic subunit, and non-catalytic beta and gamma subunits. AMPK is an important energy-sensing enzyme that monitors cellular energy status. In response to cellular metabolic stresses, AMPK is activated, and thus phosphorylates and inactivates acetyl-CoA carboxylase (ACC) and beta-hydroxy beta-methylglutaryl-CoA reductase (HMGCR), key enzymes involved in regulating de novo biosynthesis of fatty acid and cholesterol. This subunit may be a positive regulator of AMPK activity. It is highly expressed in skeletal muscle and thus may have tissue-specific roles. 1q21.1 deletion syndrome 1q21.1 duplication syndrome PRKAB2 has been shown to interact with PRKAG2 and PRKAG1. Research on the genes CHD1L and PRKAB2 within lymphoblast cells lead to the ...
Life Extension AMPK Activator Description Emulates Cell Energizing Effects of Caloric Restriction AMPK is an enzyme that serves as the bodys
The tumor suppressor kinase LKB1 has been identified as a physiologic activator of the key metabolic regulator 5-AMP-activated protein kinase, establishing a possible molecular link between the...
Hypoxic pulmonary vasoconstriction is a vital homeostatic mechanism that aids ventilation-perfusion matching in the lung, for which the underlying mechanism(s) remains controversial. However, our most recent investigations strongly suggest that hypoxic pulmonary vasoconstriction is precipitated, at least in part, by the inhibition of mitochondrial oxidative phosphorylation by hypoxia, an increase in the AMP/ATP ratio and consequent activation of AMP-activated protein kinase (AMPK). Unfortunately, these studies lacked the definitive proof that can only be provided by selectively blocking AMPK-dependent signalling cascades. The aim of the present study was, therefore, to determine the effects of the AMPK inhibitor compound C upon: (1) phosphorylation in response to hypoxia of a classical AMPK substrate, acetyl CoA carboxylase, in rat pulmonary arterial smooth muscle and (2) hypoxic pulmonary vasoconstriction in rat isolated intrapulmonary arteries. Acetyl CoA carboxylase phosphorylation was increased
TY - JOUR. T1 - AMP-activated protein kinase and hypoxic pulmonary vasoconstriction. AU - Robertson,Tom P.. AU - Mustard,Kirsteen J. W.. AU - Lewis,Tristan H.. AU - Clark,Jill H.. AU - Wyatt,Christopher N.. AU - Blanco,Elisa A.. AU - Peers,Chris. AU - Hardie,D. Grahame. AU - Evans,A. Mark. PY - 2008/10/24. Y1 - 2008/10/24. N2 - Hypoxic pulmonary vasoconstriction is a vital homeostatic mechanism that aids ventilation-perfusion matching in the lung, for which the underlying mechanism(s) remains controversial. However, our most recent investigations strongly suggest that hypoxic pulmonary vasoconstriction is precipitated, at least in part, by the inhibition of mitochondrial oxidative phosphorylation by hypoxia, an increase in the AMP/ATP ratio and consequent activation of AMP-activated protein kinase (AMPK). Unfortunately, these studies lacked the definitive proof that can only be provided by selectively blocking AMPK-dependent signalling cascades. The aim of the present study was. therefore, to ...
10) A base other than U at position 5 of the sense strand.(11) A base other than A at position 11 of the sense strand.(12) A base other than an A at position 1 of the sense strand.(13) A base other than an A at position 2 of the sense strand.(14) An A base at position 4 of the sense strand.(15) An A base at position 5 of the sense strand.(16) An A base at position 6 of the sense strand.(17) An A base at position 7 of the sense strand.(18) An A base at position 8 of the sense strand.(19) A base other than an A at position 9 of the sense strand.(20) A base other than an A at position 10 of the sense strand.(21) A base other than an A at position 11 of the sense strand.(22) A base other than an A at position 12 of the sense strand.(23) An A base at position 13 of the sense strand.(24) A base other than an A at position 14 of the sense strand.(25) An A base at position 15 of the sense strand(26) An A base at position 16 of the sense strand.(27) An A base at position 17 of the sense strand.(28) An A ...
Burkholderia stabilis strain LMG14294 histidinol-phosphate aminotransferase (hisC) gene, partial cds; imidazole glycerol phosphate dehydratase (hisB), multiple antibiotic resistance-related protein (marC), imidazole glycerol phosphate synthase glutamine amidotransferase subunit (hisH), phosphoribosylformimino-5-aminoimidazole carboxamide ribotide isomerase (hisA), imidazole glycerol phosphate synthase subunit (hisF), phosphoribosyl-AMP cyclohydrolase (hisI), and phosphoribosyl-ATP pyrophosphohydrolase (hisE) genes, complete cds; and membrane protein gene, partial ...
Burkholderia ambifaria strain LMG19467 histidinol-phosphate aminotransferase (hisC) gene, partial cds; imidazole glycerol phosphate dehydratase (hisB), multiple antibiotic resistance-related protein (marC), imidazole glycerol phosphate synthase glutamine amidotransferase subunit (hisH), phosphoribosylformimino-5-aminoimidazole carboxamide ribotide isomerase (hisA), imidazole glycerol phosphate synthase subunit (hisF), phosphoribosyl-AMP cyclohydrolase (hisI), and phosphoribosyl-ATP pyrophosphohydrolase (hisE) genes, complete cds; and membrane protein gene, partial ...

ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase)ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase)

5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase), Authors: Jean-Loup Huret. Published in: ... ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase). Written. 2001-08. Jean-Loup Huret. ... ATIC (5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase). Atlas Genet Cytogenet Oncol Haematol ... Characterization of molecularly cloned human 5-aminoimidazole-4-carboxamide ribonucleotide transformylase.. Sugita T, Aya H, ...
more infohttp://atlasgeneticsoncology.org/Genes/GC_ATIC.html

siRNA targeting 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase (ATIC) - Patent applicationsiRNA targeting 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase (ATIC) - Patent application

0030]In various embodiments, siRNAs that target 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP ... Patent application title: siRNA targeting 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase ( ... Patent application title: siRNA targeting 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase ( ...
more infohttp://www.patentsencyclopedia.com/app/20080207884

RCSB PDB 









for 1P4RRCSB PDB for 1P4R

Crystal structures of human bifunctional enzyme aminoimidazole-4-carboxamide ribonucleotide transformylase/IMP cyclohydrolase ... AMINOIMIDAZOLE 4-CARBOXAMIDE RIBONUCLEOTIDE. AICAR (Synonym). C9 H15 N4 O8 P NOTGFIUVDGNKRI-UUOKFMHZSA-N ...
more infohttp://www.rcsb.org/pdb/explore/biologyAndChemistry.do?structureId=1P4R

Impact of Genetic Variants of ATP Binding Cassette B1, AICAR Transformylase/IMP Cyclohydrolase, Folyl-polyglutamate Synthetase,...Impact of Genetic Variants of ATP Binding Cassette B1, AICAR Transformylase/IMP Cyclohydrolase, Folyl-polyglutamate Synthetase,...

Polyglutamation of methotrexate with common polymorphisms in reduced folate carrier, aminoimidazole carboxamide ribonucleotide ... phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) transformylase/inositol monophosphate (IMP) cyclohydrolase (ATIC; ...
more infohttp://reumatologiaclinica.org/en/impact-genetic-variants-atp-binding/articulo/S217357431730120X/

Structure Cluster 









- 1PL0: Crystal structure of human ATIC in complex with folate-based inhibitor, BW2315U89UC 3D...Structure Cluster - 1PL0: Crystal structure of human ATIC in complex with folate-based inhibitor, BW2315U89UC 3D...

Crystal Structures of Human Bifunctional Enzyme Aminoimidazole-4-carboxamide Ribonucleotide Transformylase/IMP Cyclohydrolase ...
more infohttp://www.rcsb.org/pdb/explore/structureCluster.do?structureId=1PL0

Inhibitory Effect of Aminoimidazole Carboxamide Ribonucleotide (AICAR) on Endotoxin-Induced Uveitis in Rats | IOVS | ARVO...Inhibitory Effect of Aminoimidazole Carboxamide Ribonucleotide (AICAR) on Endotoxin-Induced Uveitis in Rats | IOVS | ARVO...

Nath N Giri S Prasad R Salem ML Singh AK Singh I . 5-aminoimidazole-4-carboxamide ribonucleoside: a novel immunomodulator with ... Giri S Nath N Smith B Viollet B Singh AK Singh I . 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside inhibits ... Inhibitory Effect of Aminoimidazole Carboxamide Ribonucleotide (AICAR) on Endotoxin-Induced Uveitis in Rats ... Inhibitory Effect of Aminoimidazole Carboxamide Ribonucleotide (AICAR) on Endotoxin-Induced Uveitis in Rats ...
more infohttps://iovs.arvojournals.org/article.aspx?articleid=2187916

Aminoimidazole Carboxamide Ribonucleotide (AICAR) Inhibits the Growth of Retinoblastoma In Vivo by Decreasing Angiogenesis and...Aminoimidazole Carboxamide Ribonucleotide (AICAR) Inhibits the Growth of Retinoblastoma In Vivo by Decreasing Angiogenesis and...

5-Aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR), an analog of AMP is widely used as an activator of AMP-kinase ( ... Aminoimidazole Carboxamide Ribonucleotide (AICAR) Inhibits the Growth of Retinoblastoma In Vivo by Decreasing Angiogenesis and ... Aminoimidazole carboxamide ribonucleotide (AICAR) inhibits the growth of retinoblastoma in vivo by decreasing angiogenesis and ... Aminoimidazole Carboxamide Ribonucleotide (AICAR) Inhibits the Growth of Retinoblastoma In Vivo by Decreasing Angiogenesis and ...
more infohttps://dash.harvard.edu/handle/1/10612916?show=full

AICAR (5-aminoimidazole-4-carboxamide riboside) - AnabolicMinds.comAICAR (5-aminoimidazole-4-carboxamide riboside) - AnabolicMinds.com

AnabolicMinds.com , Forum , Supplement Forum , Supplements , AICAR (5-aminoimidazole-4-carboxamide riboside) ... AICAR (5-aminoimidazole-4-carboxamide riboside) No hope of ever seeing this in bulk is there? Its outrageously expensive in ...
more infohttp://anabolicminds.com/forum/supplements/26253-aicar-5-aminoimidazole.html

5-Aminoimidazole 4-Carboxamide Ribonucleotide Formyltransferase ELISA Kits | Biocompare.com5-Aminoimidazole 4-Carboxamide Ribonucleotide Formyltransferase ELISA Kits | Biocompare.com

Compare 5-Aminoimidazole 4-Carboxamide Ribonucleotide Formyltransferase ELISA Kits from leading suppliers on Biocompare. View ... 5-Aminoimidazole 4-Carboxamide Ribonucleotide Formyltransferase ELISA Kits. The ELISA (enzyme-linked immunosorbent assay) is a ... Your search returned 13 5-Aminoimidazole 4-Carboxamide Ribonucleotide Formyltransferase ELISA ELISA Kit across 5 suppliers. ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-143746/ELISA_Kit/ELISA_5-Aminoimidazole_4-Carboxamide_Ribonucleotide_Formyltransferase

Intracerebroventricular infusion of glucose, insulin, and the adenosine monophosphate-activated kinase activator, 5...Intracerebroventricular infusion of glucose, insulin, and the adenosine monophosphate-activated kinase activator, 5...

We show in this study that the intracerebroventricular infusion of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside ( ... 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside, controls muscle glycogen synthesis.. Perrin C1, Knauf C, Burcelin R. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/15192044?dopt=Abstract

Metabolomics Identifies Pyrimidine Starvation as the Mechanism of 5-Aminoimidazole-4-Carboxamide-1-β-Riboside-Induced Apoptosis...Metabolomics Identifies Pyrimidine Starvation as the Mechanism of 5-Aminoimidazole-4-Carboxamide-1-β-Riboside-Induced Apoptosis...

Aminoimidazole carboxamide ribonucleoside toxicity: a model for study of pyrimidine starvation. J Cell Physiol 1981;107:335-44. ... AICAr (5-aminoimidazole-4-carboxamide-1-β-riboside) is a nucleoside that is taken up by cells by adenosine transporters and ... 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP- ... 5-Aminoimidazole-4-carboxamide riboside induces apoptosis in Jurkat cells, but the AMP-activated protein kinase is not involved ...
more infohttp://mct.aacrjournals.org/content/12/7/1310.full

Cell cycle regulation via p53 phosphorylation by a 5-AMP activated protein kinase activator, 5-aminoimidazole- 4-carboxamide-1...Cell cycle regulation via p53 phosphorylation by a 5'-AMP activated protein kinase activator, 5-aminoimidazole- 4-carboxamide-1...

5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) is an activator of AMP activated protein kinase (AMPK) and a ... Cell cycle regulation via p53 phosphorylation by a 5-AMP activated protein kinase activator, 5-aminoimidazole- 4-carboxamide-1 ... Aminoimidazole Carboxamide/analogs & derivatives*. *Aminoimidazole Carboxamide/pharmacology*. *Carcinoma, Hepatocellular/ ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/11554766?dopt=Abstract

Augmentation of Reduced Folate Carrier-Mediated Folate/Antifolate Transport through an Antiport Mechanism with 5-Aminoimidazole...Augmentation of Reduced Folate Carrier-Mediated Folate/Antifolate Transport through an Antiport Mechanism with 5-Aminoimidazole...

5-aminoimidazole-4-carboxamide riboside. MTX. methotrexate. ZMP. 5-aminoimidazole-4-carboxamide ribotide monophosphate. 5- ... 5-aminoimidazole-4-carboxamide ribotide diphosphate. ZTP. 5-aminoimidazole-4-carboxamide ribotide triphosphate. mTOR. mammalian ... 2005) 5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside inhibits cancer cell proliferation in vitro and in vivo via AMP- ... 1981) Aminoimidazole carboxamide ribonucleoside toxicity: a model for study of pyrimidine starvation. J Cell Physiol 107:335- ...
more infohttp://molpharm.aspetjournals.org/content/82/2/209

Enhancement of insulin-mediated rat muscle glucose uptake and microvascular perfusion by 5-aminoimidazole-4-carboxamide-1-beta...Enhancement of insulin-mediated rat muscle glucose uptake and microvascular perfusion by 5-aminoimidazole-4-carboxamide-1-beta...

5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR, an activator of AMP-activated protein kinase), can also induce ... 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR, an activator of AMP-activated protein kinase), can also induce ... Enhancement of insulin-mediated rat muscle glucose uptake and microvascular perfusion by 5-aminoimidazole-4-carboxamide-1-beta- ... Enhancement of insulin-mediated rat muscle glucose uptake and microvascular perfusion by 5-aminoimidazole-4-carboxamide-1-beta- ...
more infohttps://www.garvan.org.au/research/publications/13133

Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL)...Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL)...

AICAR, 5-Aminoimidazole-4-Carboxamide-1-β-4-Ribofuranoside; AK, adenosine kinase; AMPK, AMP activated protein kinase; PI3K, ... Rattan R, Giri S, Singh AK, Singh I: 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside inhibits cancer cell proliferation ... Corton JM, Gillespie JG, Hawley SA, Hardie DG: 5-aminoimidazole-4-carboxamide ribonucleoside. A specific method for activating ... Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL ...
more infohttps://molecular-cancer.biomedcentral.com/articles/10.1186/1476-4598-6-46

Reactome | 5-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) + 10-formyltetrahydrofolate => 5-phosphoribosyl-5...Reactome | 5'-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) + 10-formyltetrahydrofolate => 5'-phosphoribosyl-5...

On the purification and mechanism of action of 5-aminoimidazole-4-carboxamide-ribonucleotide transformylase from chicken liver ... phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) and 10-formyltetrahydrofolate to form 5-phosphoribosyl-5- ... 5-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) + 10-formyltetrahydrofolate =, 5-phosphoribosyl-5-formaminoimidazole- ... 5-phosphoribosyl-5-aminoimidazole-4-carboxamide (AICAR) + 10-formyltetrahydrofolate => 5-phosphoribosyl-5-formaminoimidazole- ...
more infohttps://reactome.org/content/detail/R-GGA-419254

Requirement for Rhizobial Production of 5-Aminoimidazole-4-Carboxamide by Mary Jo Rosovitz, Jeffrey D. Newman et al."Requirement for Rhizobial Production of 5-Aminoimidazole-4-Carboxamide" by Mary Jo Rosovitz, Jeffrey D. Newman et al.

... and by examining several mutants defective in various pathways of 5-aminoimidazole-4-carboxamide ribonucleolide (AICAR) ... Exogenous application of the purine precursor 5-aminoimidazole-4-carboxamide (AICA) riboside restores infection and enhances ... Exogenous application of the purine precursor 5-aminoimidazole-4-carboxamide (AICA) riboside restores infection and enhances ... Requirement for Rhizobial Production of 5-Aminoimidazole-4-Carboxamide Ribonucleotide (AICAR) for Infection of Bean ...
more infohttps://epublications.marquette.edu/bio_fac/566/

Role of Serotonergic Agents in Primary Chronic ConstipationRole of Serotonergic Agents in Primary Chronic Constipation

Granisetron[49] (aminoimidazole carboxamide). Approved by FDA for. CINV. RINV. Dolasetron[50] (aminoimidazole carboxamide). ... Ondansetron[48] (aminoimidazole carboxamide). Antiemetic: centrally acting agents that prevent serotonin from initiating ...
more infohttps://www.medscape.com/viewarticle/518324_3

Encyclopedia of Human Nutrition.PDFEncyclopedia of Human Nutrition.PDF

aminoimidazolecarboxamide ribonucleotide; figlu, formiminoglutamic acid; IMP, inosine monophosphate.. vitamin B. 12. deficiency ... carboxamide ribonucleotide), pyrimidine nucleotide mentation of folate coenzymes between the cytosol. biosynthesis (methylation ...
more infohttp://content.yudu.com/Library/A17k4j/EncyclopediaofHumanN/resources/886.htm

Frontiers | Metabolic Reprograming of Mononuclear Phagocytes in Progressive Multiple Sclerosis | ImmunologyFrontiers | Metabolic Reprograming of Mononuclear Phagocytes in Progressive Multiple Sclerosis | Immunology

AICAR, aminoimidazole carboxamide ribonucleotide; cis-aco, cis-aconitase; DMF, dimethyl fumarate; HIF, hypoxia-inducible factor ... Indeed, metformin and 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR), well-established AMPk activators can ...
more infohttps://www.frontiersin.org/articles/10.3389/fimmu.2015.00106/full

Phosphoribosylaminoimidazolecarboxamide formyltransferase - WikipediaPhosphoribosylaminoimidazolecarboxamide formyltransferase - Wikipedia

The systematic name of this enzyme class is 10-formyltetrahydrofolate:5-phosphoribosyl-5-amino-4-imidazole-carb oxamide N- ... aminoimidazolecarboxamide ribonucleotide transformylase, and. *transformylase,. *bifunctional purine biosynthesis protein PURH, ...
more infohttps://en.wikipedia.org/wiki/Phosphoribosylaminoimidazolecarboxamide_formyltransferase

hisA - 1-(5-phosphoribosyl)-5-[(5-phosphoribosylamino)methylideneamino] imidazole-4-carboxamide isomerase - Xylella fastidiosa ...hisA - 1-(5-phosphoribosyl)-5-[(5-phosphoribosylamino)methylideneamino] imidazole-4-carboxamide isomerase - Xylella fastidiosa ...

Phosphoribosylformimino-5-aminoimidazole carboxamide ribotide isomerase. ,p>This subsection of the ,a href="http://www.uniprot. ... 1-(5-phosphoribosyl)-5-[(5-phosphoribosylamino)methylideneamino] imidazole-4-carboxamide isomerase (EC:5.3.1.16). Alternative ... 1-(5-phosphoribosyl)-5-[(5-phosphoribosylamino)methylideneamino] imidazole-4-carboxamide isomeraseAdd BLAST. 265. ... 1-(5-phospho-beta-D-ribosyl)-5-((5-phospho-beta-D-ribosylamino)methylideneamino)imidazole-4-carboxamide = 5-((5-phospho-1-deoxy ...
more infohttp://www.uniprot.org/uniprot/Q9PBC9

KEGG BRITE: KEGG Orthology (KO) - Acinetobacter baumannii AYEKEGG BRITE: KEGG Orthology (KO) - Acinetobacter baumannii AYE

ABAYE0250 hisA; phosphoribosylformimino-5-aminoimidazole carboxamide isomerase ABAYE0253 hisH; imidazole glycerol phosphate ... phosphoribosylformimino-5-aminoimidazole carboxamide ribotide isomerase [EC:5.3.1.16] K02501 hisH; glutamine amidotransferase [ ...
more infohttp://www.genome.jp/kegg-bin/get_htext?aby00001+ABAYE2333
  • Another feature glycinamide ribonucleotide and 5-amino-4-imidazole of intracellular folate metabolism is the compart- carboxamide ribonucleotide), pyrimidine nucleotide mentation of folate coenzymes between the cytosol biosynthesis (methylation of deoxyuridylic acid to thy- and the mitochondria. (yudu.com)
  • CEDDIA, Rolando B. Loss of the anorexic response to systemic 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside administration despite reducing hypothalamic AMP-activated protein kinase phosphorylation in insulin- deficient rats. (usp.br)
  • In most organisms steps 9 and 10 are catalyzed by the purH gene product, a bifunctional enzyme with both 5-formaminoimidazole-4-carboxamide ribonucleotide (FAICAR) synthase and inosine monophosphate (IMP) cyclohydrolase activity. (rcsb.org)