Search results for "clase"

AbstractIn the yeast Saccharomyces cerevisiae the genes involved in galactose metabolism (GAL1,7,10) are transcriptionally activated more than a 1000-fold in the presence of galactose as the sole carbon source in the culture media. In the present work, we monitored the activity of the GAL10 gene promoter in different Ras-cAMP genetic backgrounds. We demonstrate that overexpression of C-terminus of the nucleotide exchange factor Cdc25p stimulates GAL10 transcription in yeast strains carrying the contemporary deletion of both RAS genes. Moreover, the deletion of the chromosomal CDC25 gene provokes impaired growth on galactose based media in yeast strain lacking both RAS genes and adenylate cy…

Galactose metabolismSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeBiophysicsGene ExpressionSaccharomyces cerevisiaeRas glucose and galactose metabolism cancerGTP-binding proteinSignal transductionBiochemistryLeloir pathwaychemistry.chemical_compoundRas-GRF1Protein kinase AStructural BiologyGenes ReporterGene Expression Regulation FungalGeneticsRNA MessengerProtein kinase APromoter Regions GeneticMolecular BiologyChromosomal DeletionAllelesbiologyras-GRF1GalactosePromoterCell Biologybiology.organism_classificationLeloir pathwayExchange factorPhenotypechemistryBiochemistryGalactoseras ProteinsSignal transductionGene DeletionAdenylyl CyclasesPlasmidsFEBS Letters

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Nitric Oxide/Cyclic Guanosine Monophosphate Signaling via Guanylyl Cyclase Isoform 1 Mediates Early Changes in Synaptic Transmission and Brain Edema …

2021

Traumatic brain injury (TBI) often induces structural damage, disruption of the blood-brain barrier (BBB), neurodegeneration, and dysfunctions of surviving neuronal networks. Nitric oxide (NO) signaling has been suggested to affect brain functions after TBI. The NO exhibits most of its biological effects by activation of the primary targets-guanylyl cyclases (NO-GCs), which exists in two isoforms (NO-GC1 and NO-GC2), and the subsequently produced cyclic guanosine monophosphate (cGMP). However, the specific function of the NO-NO-GCs-cGMP pathway in the context of brain injury is not fully understood. To investigate the specific role of the isoform NO-GC1 early after brain injuries, we perfor…

Gene isoform030506 rehabilitationTraumatic brain injuryBrain EdemaReceptors Cell SurfaceNeurotransmissionBlood–brain barrierNitric OxideSynaptic TransmissionNitric oxide03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineBrain Injuries TraumaticmedicinePremovement neuronal activityAnimalsCyclic guanosine monophosphateCyclic GMPMice KnockoutNeurodegenerationSomatosensory Cortexmedicine.diseaseIsoenzymesmedicine.anatomical_structurenervous systemchemistryGuanylate CyclaseNeurology (clinical)0305 other medical scienceNeuroscience030217 neurology & neurosurgerySignal TransductionJournal of neurotrauma

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Nitric Oxide: Biological Synthesis and Functions

2012

The pluripotent gaseous messenger molecule nitric oxide (NO) controls vital functions such as neurotransmission or vascular tone (via activation of soluble guanylyl cyclase), gene transcription, mRNA translation (via iron-responsive elements), and post-translational modifications of proteins (via ADP-ribosylation). In higher concentrations, NO is capable of destroying parasites and tumor cells by inhibiting iron-containing enzymes or directly interacting with the DNA of these cells. In view of this multitude of functions of NO, it is important to understand the mechanisms by which cells accomplish and regulate the production of this molecule. In mammals, three isozymes of NO synthase (NOS; …

Gene isoformNADPH oxidasebiologyNeurodegenerationInflammationmedicine.diseaseIsozymeNitric oxideCell biologychemistry.chemical_compoundchemistrymedicinebiology.proteinmedicine.symptomSoluble guanylyl cyclasePeroxynitrite

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Effects of histamine on dentate granule cells in vitro

1990

Abstract Hippocampal slices from rat brain were exposed to histamine and related substances in a perfusion chamber. Granule cells of the dentate gyrus were studied with conventional extra- and intracellular recording and a single electrode voltage clamp. Histamine caused, through activation of H 2 -receptors, a small depolarization, an increase in the number of synaptic and action potentials, a block of the long lasting (but not the early) component of spike afterhyperpolarizations and a reduction of the accommodation of action potential firing. These effects were mimicked by forskolin (suggests activation of adenylate cyclase). In voltage clamp, histamine blocked a long lasting calcium-dep…

General NeuroscienceDentate gyrusColforsinHistaminergicAction PotentialsRats Inbred StrainsIn Vitro TechniquesPerforant pathInhibitory postsynaptic potentialHippocampusMembrane PotentialsRatschemistry.chemical_compoundmedicine.anatomical_structurechemistryHistamine H2 receptormedicineExcitatory postsynaptic potentialBiophysicsAnimalsHistamine H3 receptorNeuroscienceHistamineAdenylyl CyclasesHistamineNeuroscience

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