Search results for "HUMDISEASE"

showing 6 items of 6 documents

Ofd1, a Human Disease Gene, Regulates the Length and Distal Structure of Centrioles

2010

SUMMARYCentrosomes and their component centrioles represent the principal microtubule organizing centers of animal cells. Here we show that the gene underlying Orofaciodigital Syndrome 1, Ofd1, is a component of the distal centriole that controls centriole length. In the absence of Ofd1, distal regions of centrioles, but not procentrioles, elongate abnormally. These long centrioles are structurally similar to normal centrioles, but contain destabilized microtubules with abnormal post-translational modifications. Ofd1 is also important for centriole distal appendage formation and centriolar recruitment of the intraflagellar transport protein Ift88. To model OFD1 Syndrome in embryonic stem ce…

G2 PhaseCentrioleMicrotubule-associated proteinMutation MissenseHUMDISEASECell Cycle ProteinsBiologyMicrotubulesModels BiologicalArticleGeneral Biochemistry Genetics and Molecular BiologyCentriole elongationCell LineMiceIntraflagellar transportCiliogenesisAnimalsHumansBasal bodyMolecular BiologyEmbryonic Stem CellsCentriolesTumor Suppressor ProteinsProteinsCell BiologyOrofaciodigital SyndromesPhosphoproteinsRecombinant ProteinsCell biologyCentrosomeCELLBIOCentriolar satelliteMicrotubule-Associated ProteinsDevelopmental Biology
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Telomerase Reverse Transcriptase Delays Aging in Cancer-Resistant Mice

2008

Summary Telomerase confers limitless proliferative potential to most human cells through its ability to elongate telomeres, the natural ends of chromosomes, which otherwise would undergo progressive attrition and eventually compromise cell viability. However, the role of telomerase in organismal aging has remained unaddressed, in part because of the cancer-promoting activity of telomerase. To circumvent this problem, we have constitutively expressed telomerase reverse transcriptase (TERT), one of the components of telomerase, in mice engineered to be cancer resistant by means of enhanced expression of the tumor suppressors p53, p16, and p19ARF. In this context, TERT overexpression improves …

KeratinocytesAgingTelomeraseCell SurvivalTransgeneHUMDISEASEMice TransgenicContext (language use)BiologyModels BiologicalGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyMiceNeoplasmsmedicineAnimalsHumansTelomerase reverse transcriptaseViability assayInsulin-Like Growth Factor ITelomeraseRegulation of gene expressionBiochemistry Genetics and Molecular Biology(all)Stem CellsCancermedicine.diseaseMolecular biologyTelomereGene Expression Regulation NeoplasticCancer researchCELLBIOEpidermisCell
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The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

2006

SummaryBalanced control of neuronal activity is central in maintaining function and viability of neuronal circuits. The endocannabinoid system tightly controls neuronal excitability. Here, we show that endocannabinoids directly target hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice. Functional CB1 cannabinoid receptors are present on glutamatergic terminals of the hippocampal formation, colocalizing with vesicular glutamate transporter 1 (VGluT1). Conditional deletion of the CB1 gene either in cortical glutamatergic neurons or in forebrain GABAergic neurons, as well as virally induced deletion of the CB1 gene in the hippocampus, demonstrat…

MaleVesicular glutamate transporter 1HUMDISEASEHippocampusGene ExpressionHippocampal formationHippocampusMembrane Potentialschemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1Premovement neuronal activitygamma-Aminobutyric Acid0303 health sciencesKainic AcidbiologyBehavior AnimalReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyGeneral NeurosciencePyramidal CellsCalcium Channel BlockersEndocannabinoid systemlipids (amino acids peptides and proteins)psychological phenomena and processesmedicine.drugKainic acidNeuroscience(all)MorpholinesGlutamic AcidMice TransgenicNaphthalenesMOLNEUROgamma-Aminobutyric acid03 medical and health sciencesGlutamatergicCannabinoid Receptor ModulatorsmedicineAnimals030304 developmental biologyAnalysis of VarianceEpilepsyBenzoxazinesMice Inbred C57BLnervous systemchemistryCalcium-Calmodulin-Dependent Protein KinasesVesicular Glutamate Transport Protein 1biology.proteinNerve NetSYSNEUROCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroscience030217 neurology & neurosurgeryEndocannabinoidsNeuron
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Paracrine Activation of Hepatic CB1 Receptors by Stellate Cell-Derived Endocannabinoids Mediates Alcoholic Fatty Liver

2008

SummaryAlcohol-induced fatty liver, a major cause of morbidity, has been attributed to enhanced hepatic lipogenesis and decreased fat clearance of unknown mechanism. Here we report that the steatosis induced in mice by a low-fat, liquid ethanol diet is attenuated by concurrent blockade of cannabinoid CB1 receptors. Global or hepatocyte-specific CB1 knockout mice are resistant to ethanol-induced steatosis and increases in lipogenic gene expression and have increased carnitine palmitoyltransferase 1 activity, which, unlike in controls, is not reduced by ethanol treatment. Ethanol feeding increases the hepatic expression of CB1 receptors and upregulates the endocannabinoid 2-arachidonoylglycer…

Malemedicine.medical_specialtyPhysiologyHUMDISEASEArachidonic AcidsGlyceridesMiceCarnitine palmitoyltransferase 1PiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsParacrine CommunicationmedicineAnimalsReceptorDiet Fat-RestrictedMolecular BiologyCells CulturedMice KnockoutCarnitine O-PalmitoyltransferaseEthanolChemistryLipogenesisFatty AcidsFatty liverCell Biologymedicine.diseaseEndocannabinoid systemCoculture TechniquesUp-RegulationMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologyLiverLipogenesisHepatocytesHepatic stellate cellPyrazoleslipids (amino acids peptides and proteins)Alcoholic fatty liverFatty Acid SynthasesRimonabantSteatosisSterol Regulatory Element Binding Protein 1Oxidation-ReductionEndocannabinoidsFatty Liver AlcoholicCell Metabolism
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Cooperation of Two mRNA-Binding Proteins Drives Metabolic Adaptation to Iron Deficiency

2008

Summary Iron (Fe) is an essential cofactor for a wide range of cellular processes. We have previously demonstrated in yeast that Cth2 is expressed during Fe deficiency and promotes degradation of a battery of mRNAs leading to reprogramming of Fe-dependent metabolism and Fe storage. We report here that the Cth2-homologous protein Cth1 is transiently expressed during Fe deprivation and participates in the response to Fe deficiency through the degradation of mRNAs primarily involved in mitochondrially localized activities including respiration and amino acid biosynthesis. In parallel, wild-type cells, but not cth1 Δ cth2 Δ cells, accumulate mRNAs encoding proteins that function in glucose impo…

Saccharomyces cerevisiae ProteinsPhysiologySaccharomyces cerevisiaeHUMDISEASERNA-binding proteinSaccharomyces cerevisiaeProtein Serine-Threonine KinasesDNA-binding proteinArticlechemistry.chemical_compoundTristetraprolinGlucose importRNA MessengerPhosphorylationProtein kinase AMolecular BiologybiologyGlycogenRNA-Binding ProteinsIron DeficienciesCell BiologyMetabolismbiology.organism_classificationAdaptation PhysiologicalDNA-Binding ProteinsMetabolismBiochemistrychemistryPhosphorylationTranscription FactorsCell Metabolism
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CB(1) signaling in forebrain and sympathetic neurons is a key determinant of endocannabinoid actions on energy balance

2010

The endocannabinoid system (ECS) plays a critical role in obesity development. The pharmacological blockade of cannabinoid receptor type 1 (CB(1)) has been shown to reduce body weight and to alleviate obesity-related metabolic disorders. An unsolved question is at which anatomical level CB(1) modulates energy balance and the mechanisms involved in its action. Here, we demonstrate that CB(1) receptors expressed in forebrain and sympathetic neurons play a key role in the pathophysiological development of diet-induced obesity. Conditional mutant mice lacking CB(1) expression in neurons known to control energy balance, but not in nonneuronal peripheral organs, displayed a lean phenotype and res…

Sympathetic Nervous SystemPhysiologymedicine.medical_treatmentHUMDISEASEFluorescent Antibody TechniqueBody TemperatureMice0302 clinical medicineReceptor Cannabinoid CB1Cannabinoid receptor type 1ReceptorIn Situ HybridizationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionCB(1)ThermogenesisEndocannabinoid systemOBESITYCB1 knock outlipids (amino acids peptides and proteins)CB(1); CANNABINOID RECEPTOR; OBESITY; ENDOCANNABINOID SYSTEM; METABOLIC DISORDERSSignal Transductionmedicine.medical_specialtyforebrainImmunoblottingCitrate (si)-SynthaseIn situ hybridizationHyperphagiaBiologyDNA MitochondrialModels BiologicalENDOCANNABINOID SYSTEMMOLNEURONO03 medical and health sciencesProsencephalonLipid oxidationInternal medicineMETABOLIC DISORDERSmedicineAnimalsMolecular BiologyCANNABINOID RECEPTOR030304 developmental biologyAnalysis of VarianceX-Ray MicrotomographyCell Biologyendocannabinoidenergy balanceEndocrinologynervous systemsympathetic neuronsForebrainCannabinoidEnergy Metabolismendocannabinoid; forebrain; sympathetic neurons; energy balance; CB1 knock outNeuroscienceThermogenesis030217 neurology & neurosurgery
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