Search results for "Aminoimidazole Carboxamide"

showing 5 items of 5 documents

Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

2016

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the auto…

0301 basic medicineCachexiaColorectal cancerMuscle Fibers SkeletalMicevoluntary physical activityChloroquineMice Inbred BALB CMultidisciplinaryMuscle WeaknessMyogenesis3. Good healthmedicine.anatomical_structureColonic NeoplasmsFemalecancer cachexiamedicine.drugmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/Cancerautophagic fluxBiologyArticleCachexia03 medical and health sciencesAtrophyInternal medicineCell Line TumorPhysical Conditioning AnimalmedicineAutophagyAerobic exerciseAnimalsHumansMuscle SkeletalSirolimusrapamycinAutophagyAutophagosomesSkeletal musclemuscle wasting[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyRibonucleotidesmedicine.diseaseAminoimidazole CarboxamideSurvival Analysisexercise mimetics030104 developmental biologyEndocrinology5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR)LysosomesNeoplasm Transplantationmuscle wasting; cancer cachexia; voluntary physical activity; exercise mimetics; 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR); rapamycin; autophagic flux
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Metabolomics of the effect of AMPK activation by AICAR on human umbilical vein endothelial cells

2011

AMP-activated protein kinase (AMPK) is a metabolic master switch expressed in a great number of cells and tissues. AMPK is thought to modulate the cellular response to different stresses that increase cellular AMP concentration. The adenosine analog, 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) is an AMPK activator used in many studies to assess the effects of AMPK activation on cellular metabolism and function. However, the effect of AICAR on cell metabolism reaches many different pathways and metabolites, some of which do not seem to be fully related to AMPK activation. We have now for the first time used NMR metabolomics on human umbilical vein endothelial cells (HUVEC) fo…

Citric Acid CycleMetabolic networkAMP-Activated Protein KinasesBiologyUmbilical veinMetabolomicsHuman Umbilical Vein Endothelial CellsGeneticsmedicineHumansMetabolomicsProtein kinase ANuclear Magnetic Resonance BiomolecularCells CulturedPhospholipidsAnalysis of VarianceActivator (genetics)AMPKGeneral MedicineMetabolismAminoimidazole CarboxamideAdenosineCell biologyEnzyme ActivationBiochemistryMetabolomeRibonucleosidesGlycolysisMetabolic Networks and Pathwaysmedicine.drugInternational Journal of Molecular Medicine
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AICA-ribosiduria due to ATIC deficiency: Delineation of the phenotype with three novel cases, and long-term update on the first case.

2020

5-Amino-4-imidazolecarboxamide-ribosiduria (AICA)-ribosiduria is an exceedingly rare autosomal recessive condition resulting from the disruption of the bifunctional purine biosynthesis protein PURH (ATIC), which catalyzes the last two steps of de novo purine synthesis. It is characterized biochemically by the accumulation of AICA-riboside in urine. AICA-ribosiduria had been reported in only one individual, 15 years ago. In this article, we report three novel cases of AICA-ribosiduria from two independent families, with two novel pathogenic variants in ATIC. We also provide a clinical update on the first patient. Based on the phenotypic features shared by these four patients, we define AICA-…

Hydroxymethyl and Formyl TransferasesMalemedicine.medical_specialtyCyclohydrolase activityBioinformaticsCongenital AbnormalitiesEpilepsyMultienzyme ComplexesIntellectual DisabilityGeneticsmedicineHumansBifunctional Purine Biosynthesis Protein PURHChildGenetics (clinical)ATIC DEFICIENCYEpilepsybusiness.industryInfant NewbornInfantmedicine.diseaseAminoimidazole CarboxamidePhenotypePhenotypeNucleotide DeaminasesChild PreschoolMutationMedical geneticsFemaleRibonucleosidesNephrocalcinosisbusinessRare diseaseJournal of inherited metabolic diseaseREFERENCES
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Suppression of the JNK Pathway by Induction of a Metabolic Stress Response Prevents Vascular Injury and Dysfunction

2008

Background— Oxidative injury and dysfunction of the vascular endothelium are early and causal features of many vascular diseases. Single antioxidant strategies to prevent vascular injury have met with mixed results. Methods and Results— Here, we report that induction of a metabolic stress response with adenosine monophosphate kinase (AMPK) prevents oxidative endothelial cell injury. This response is characterized by stabilization of the mitochondrion and increased mitochondrial biogenesis, resulting in attenuation of oxidative c-Jun N-terminal kinase (JNK) activation. We report that peroxisome proliferator coactivator 1α is a key downstream target of AMPK that is both necessary and suffici…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliumMitochondrionmedicine.disease_causeArticleMiceInternal medicinePhysiology (medical)Chlorocebus aethiopsmedicineAnimalsHumansVascular DiseasesRNA Small InterferingEndothelial dysfunctionHeat-Shock ProteinsMembrane Potential MitochondrialCell Deathbusiness.industryAdenylate KinaseJNK Mitogen-Activated Protein KinasesEndothelial CellsAMPKHydrogen PeroxideRibonucleotidesAminoimidazole CarboxamideOxidantsmedicine.diseaseAdaptation PhysiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAngiotensin IICell biologyMice Inbred C57BLEndothelial stem cellOxidative Stressmedicine.anatomical_structureEndocrinologyMitochondrial biogenesisMutagenesisCOS CellsbusinessCardiology and Cardiovascular MedicineOxidative stressTranscription FactorsCirculation
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Evaluation of Fused Pyrrolothiazole Systems as Correctors of Mutant CFTR Protein.

2021

Cystic fibrosis (CF) is a genetic disease caused by mutations that impair the function of the CFTR chloride channel. The most frequent mutation, F508del, causes misfolding and premature degradation of CFTR protein. This defect can be overcome with pharmacological agents named “correctors”. So far, at least three different classes of correctors have been identified based on the additive/synergistic effects that are obtained when compounds of different classes are combined together. The development of class 2 correctors has lagged behind that of compounds belonging to the other classes. It was shown that the efficacy of the prototypical class 2 corrector, the bithiazole corr-4a, could be impr…

Yellow fluorescent proteinProtein FoldingCystic FibrosisMutantPharmaceutical ScienceCystic Fibrosis Transmembrane Conductance RegulatorCarboxamidemedicine.disease_cause01 natural sciencesAnalytical Chemistrychemistry.chemical_compoundMutant ProteinDrug DiscoveryMoietyCFTR potentiatorCFTRchemistry.chemical_classification0303 health sciencesMutationbiologyChemistryChemistry (miscellaneous)Chloride channelMolecular MedicineHumanStereochemistrymedicine.drug_classCFTR correctorArticleF508del-CFTRlcsh:QD241-44103 medical and health scienceslcsh:Organic chemistrymedicineHumansBenzodioxolesPhysical and Theoretical ChemistryThiazoleCystic Fibrosi030304 developmental biology010405 organic chemistryOrganic ChemistryAminoimidazole Carboxamide0104 chemical sciencesThiazolesMutationbiology.proteinMutant ProteinsBenzodioxoleTricyclicMolecules (Basel, Switzerland)
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