Search results for "KINASE"

showing 10 items of 2635 documents

Up-Regulation of leucocytes Genes Implicated in Telomere Dysfunction and Cellular Senescence Correlates with Depression and Anxiety Severity Scores

2012

BACKGROUND: Major depressive disorder (MDD) is frequently associated with chronic medical illness responsible of increased disability and mortality. Inflammation and oxidative stress are considered to be the major mediators of the allostatic load, and has been shown to correlate with telomere erosion in the leucocytes of MDD patients, leading to the model of accelerated aging. However, the significance of telomere length as an exclusive biomarker of aging has been questioned on both methodological and biological grounds. Furthermore, telomeres significantly shorten only in patients with long lasting MDD. Sensitive and dynamic functional biomarkers of aging would be clinically useful to eval…

AgingGene Expressionlcsh:MedicineAnxietySocial and Behavioral Sciences0302 clinical medicineBiomarkers of agingMolecular Cell BiologyLeukocytesPathologyPsychologylcsh:ScienceCellular SenescenceDepression (differential diagnoses)Psychiatry0303 health sciencesMultidisciplinaryDepressionChromosome BiologyGenomicsMiddle AgedTelomereAllostatic loadUp-RegulationTelomeresMental HealthMedicineMajor depressive disorderAnxietyBiomarker (medicine)Femalemedicine.symptomResearch ArticleAdultSenescenceClinical PathologyPsychological StressBiologybehavioral disciplines and activitiesMolecular Genetics03 medical and health sciencesDiagnostic Medicinemental disordersGeneticsmedicineHumansBiologyCyclin-Dependent Kinase Inhibitor p16030304 developmental biologyDepressive Disorder Majorlcsh:RComputational BiologyHuman GeneticsDNAmedicine.diseaseTelomereOxygenGene Expression RegulationImmunologyStathminlcsh:QBiomarkers030217 neurology & neurosurgeryDNA DamagePLoS ONE
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Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells.

2014

The hematopoietic system declines with age. Myeloid-biased differentiation and increased incidence of myeloid malignancies feature aging of hematopoietic stem cells (HSCs), but the mechanisms involved remain uncertain. Here, we report that 4-mo-old mice deleted for transcription intermediary factor 1γ (Tif1γ) in HSCs developed an accelerated aging phenotype. To reinforce this result, we also show that Tif1γ is down-regulated in HSCs during aging in 20-mo-old wild-type mice. We established that Tif1γ controls TGF-β1 receptor (Tgfbr1) turnover. Compared with young HSCs, Tif1γ(-/-) and old HSCs are more sensitive to TGF-β signaling. Importantly, we identified two populations of HSCs specifical…

AgingMyeloidReceptor Transforming Growth Factor-beta Type IReceptors Cell SurfaceCell SeparationBiologyProtein Serine-Threonine KinasesTransforming Growth Factor beta1MiceSignaling Lymphocytic Activation Molecule Family Member 1Antigens CDmedicineAnimalsMyeloid CellsRNA MessengerPolyubiquitinTranscription factorCellular SenescenceRegulation of gene expressionMultidisciplinaryUbiquitinationhemic and immune systemsBiological SciencesHematopoietic Stem CellsCell biologyHematopoiesisHaematopoiesismedicine.anatomical_structurePhysiological AgingPhenotypeGene Expression RegulationSignal transductionStem cellCell agingReceptors Transforming Growth Factor betaSignal TransductionTranscription FactorsProceedings of the National Academy of Sciences of the United States of America
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Tor-Sch9 deficiency activates catabolism of the ketone body-like acetic acid to promote trehalose accumulation and longevity

2014

In mammals, extended periods of fasting leads to the accumulation of blood ketone bodies including acetoacetate. Here we show that similar to the conversion of leucine to acetoacetate in fasting mammals, starvation conditions induced ketone body-like acetic acid generation from leucine in S. cerevisiae. Whereas wild-type and ras2Δ cells accumulated acetic acid, long-lived tor1Δ and sch9Δ mutants rapidly depleted it through a mitochondrial acetate CoA transferase-dependent mechanism, which was essential for lifespan extension. The sch9Δ-dependent utilization of acetic acid also required coenzyme Q biosynthetic genes and promoted the accumulation of intracellular trehalose. These results indi…

AgingSaccharomyces cerevisiae ProteinsKetoneLongevitySaccharomyces cerevisiaeSaccharomyces cerevisiaePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAcetic acidSettore BIO/13 - Biologia ApplicataHumans2. Zero hungerchemistry.chemical_classificationbiologyCatabolismaging yeast nutrition acetic acid nutrientsTrehaloseOriginal ArticlesCell Biologybiology.organism_classificationchronological lifespanTrehaloseacetic acidSch9chemistryBiochemistryCoenzyme Q – cytochrome c reductaseKetone bodiesleucineLeucineProtein KinasesAging Cell
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Telomere Shortening in Neural Stem Cells Disrupts Neuronal Differentiation and Neuritogenesis

2009

Proliferation in the subependymal zone (SEZ) and neurogenesis in the olfactory bulb decline in the forebrain of telomerase-deficient mice. The present work reveals additional effects of telomere shortening on neuronal differentiation, as adult multipotent progenitors with critically short telomeres yield reduced numbers of neurons that, furthermore, exhibit underdeveloped neuritic arbors. Genetic data indicate that the tumor suppressor protein p53 not only mediates the adverse effects of telomere attrition on proliferation and self-renewal but it is also involved in preventing normal neuronal differentiation of adult progenitors with dysfunctional telomeres. Interestingly, progenitor cells …

AgingTelomeraseRHOANeurogenesisNotch signaling pathwayBiologyMice03 medical and health sciencesFetus0302 clinical medicineNeuritesSubependymal zoneAnimalsTelomeraseCells Cultured030304 developmental biologyMice KnockoutNeuronsrho-Associated Kinases0303 health sciencesReceptors NotchStem CellsGeneral NeuroscienceNeurogenesisCell DifferentiationArticlesTelomereNeural stem cellOlfactory bulbTelomereMice Inbred C57BLAnimals Newbornbiology.proteinTumor Suppressor Protein p53Neuroscience030217 neurology & neurosurgerySignal TransductionThe Journal of Neuroscience
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Insulin-activated Akt rescues Aβ oxidative stress-induced cell death by orchestrating molecular trafficking

2011

Increasing evidence indicates that Alzheimer's disease, one of the most diffused aging pathologies, and diabetes may be related. Here, we demonstrate that insulin signalling protects LAN5 cells by amyloid-β42 (Aβ)-induced toxicity. Aβ affects both activation of insulin receptors and the levels of phospho-Akt, a critical signalling molecule in this pathway. In contrast, oxidative stress induced by Aβ can be antagonized by active Akt that, in turn, inhibits Foxo3a, a pro-apoptotic transcription factor activated by reactive oxygen species generation. Insulin cascade protects against mitochondrial damage caused by Aβ treatment, restoring the mitochondrial membrane potential. Moreover, we show t…

AgingbiologyAmyloid betaInsulinmedicine.medical_treatmentCell BiologyMitochondrionmedicine.disease_causeCell biologyInsulin receptormedicinebiology.proteinPhosphorylationSignal transductionProtein kinase BOxidative stressAging Cell
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Protein kinase activities associated with ribosomes of developing rat brain. Identification of eukaryotic initiation factor 2 kinases.

1986

Protein kinases associated with ribosomes in the brains of suckling (4-10 days) and adult (2 months) rats were extracted from ribosomal fraction with 0.5 M KCl. The different protein kinase activities were characterized by their ability to phosphorylate three exogenous substrates: casein, histone IIs and histone IIIs in the presence of different modulators. Ribosomal salt wash fractions contain a high casein kinase activity which was partially inhibited by heparin and stimulated by calmodulin in the presence of Ca2+, indicating the presence of casein kinase I and II and calcium/calmodulin-dependent kinases. Cyclic AMP and cyclic GMP-dependent kinases and protein kinase C (calcium/phospholip…

AgingbiologyCyclin-dependent kinase 2BrainCaseinsRats Inbred StrainsMitogen-activated protein kinase kinaseRatseIF-2 KinaseDevelopmental NeuroscienceBiochemistryCasein Kinase ICasein kinase 2 alpha 1biology.proteinAnimalsASK1Cyclin-dependent kinase 9Casein kinase 1Casein kinase 2PhosphorylationProtein KinasesRibosomesDevelopmental BiologySubcellular FractionsInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
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Morphological and biochemical effects of glucocorticoids in chick embryo hepatocytes during development

1988

Abstract The administration in ovo of hydrocortisone-21-phosphate caused, in chick embryo liver, a reduction of the number of hepatocytes which can be isolated from 1 mg dry weight of liver and a marked increase of their size. Moreover, the treatment diminished the incorporation of thymidine into acid-insoluble fraction in these cells whilst it augmented the content of protein, RNA, DNA and the level of thymidine kinase/cell. These effects were highest at 8–10 days, then declined with the age, disappearing after 18th day of incubation. Similar effects were obtained by injecting other glucocorticoids or ACTH. Combined treatment with metopirone abolished the effects found with ACTH, but did n…

Agingmedicine.medical_specialtyHydrocortisoneChick EmbryoBiologyPeptide hormoneIn ovoThymidine Kinasebiochemical effectschemistry.chemical_compoundAdrenocorticotropic HormoneInternal medicinemedicineAnimalsGlucocorticoidsIncubationEmbryogenesisEmbryoMetyraponeEndocrinologyLiverchemistryThymidine kinaseThymidineGlucocorticoidDevelopmental Biologymedicine.drug
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Phosphatidylserine counteracts physiological and pharmacological suppression of humoral immune response

1990

Phosphatidylserine (PS) is a necessary cofactor for protein kinase C (PKC) activation, and changes in the synthesis of PS have been shown to participate in the mechanism(s) involved in the transmembrane signaling of interleukin 1 (IL-1). In view of the age-associated defects in T-cell functions, in the present study we have addressed the question of whether an in vivo treatment with PS might interfere with such processes. Furthermore, the effect of an in vitro treatment with PS in human peripheral blood monocytes (PBMC) or splenocytes activated with a lectin mitogen, on the expression of IL-2 receptor, was assessed. While the process of ageing was accompanied by a marked decline of humoral …

Agingmedicine.medical_specialtyReceptor expressionPhosphatidylserinesIn Vitro Techniqueschemistry.chemical_compoundImmune systemInternal medicineImmune TolerancemedicineAnimalsHumansReceptorProtein Kinase CProtein kinase CPharmacologybiologyInterleukinRats Inbred StrainsReceptors Interleukin-2PhosphatidylserineRatsEndocrinologychemistryHumoral immunityLeukocytes Mononuclearbiology.proteinFemaleAntibodySpleenImmunopharmacology
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Lipocalin-2 Regulates Hippocampal Microglial Activation in Poststroke Depression

2021

Background and Purpose: Microglia play important role in poststroke depression (PSD), however, the exact mechanism was still unclear. The purpose of the study was to study the mechanism of microglial activation in PSD.Methods: 24 rats were randomly divided into three groups: the PSD group (n = 10), the poststroke (PS) group (n = 7), and the sham group (n = 7). Primary hippocampal microglia were isolated and cultured, and recombined LCN2 protein was used to stimulate the cultured microglia. The protein expression of Iba1, P38 MAPK and PP38 MAPK was analyzed by western blotting; the LCN2 expression was measured by RT-qPCR, the serum LCN2 level and the NO level were analyzed by ELISA.Results: …

Agingpoststroke depression (PSD)nervous systemCognitive NeuroscienceAging NeurosciencemicrogliahippocampiLipocalin-2 (Lcn2)Neurosciences. Biological psychiatry. Neuropsychiatryp38 mitogen-activated protein kinase (p38 MAPK)psychological phenomena and processesOriginal ResearchRC321-571Frontiers in Aging Neuroscience
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Agonist-induced formation of FGFR1 homodimers and signaling differ among members of the FGF family

2011

Fibroblast growth factor receptor 1 (FGFR1) is known to be activated by homodimerization in the presence of both the FGF agonist ligand and heparan sulfate glycosaminoglycan. FGFR1 homodimers in turn trigger a variety of downstream signaling cascades via autophosphorylation of tyrosine residues in the cytoplasmic domain of FGFR1. By means of Bioluminescence Energy Resonance Transfer (BRET) as a sign of FGFR1 homodimerization, we evaluated in HEK293T cells the effects of all known FGF agonist ligands on homodimer formation. A significant correlation between BRET(2) signaling and ERK1/2 phosphorylation was observed, leading to a further characterization of the binding and signaling properties…

AgonistMAPK/ERK pathwaymedicine.drug_classBiophysicsSettore BIO/11 - Biologia MolecolareBiologyLigandsFibroblast growth factorSettore BIO/09 - FisiologiaBiochemistrychemistry.chemical_compoundFluorescence Resonance Energy TransfermedicineHumansReceptor Fibroblast Growth Factor Type 1Molecular BiologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Fibroblast growth factor receptor 1HEK 293 cellsAutophosphorylationCell BiologyHeparan sulfateFibroblast growth factors FGFR1 Homodimerization BRET MAPKCell biologyFibroblast Growth Factorsstomatognathic diseasesHEK293 CellschemistrySettore BIO/14 - FarmacologiaPhosphorylationHeparitin SulfateProtein MultimerizationBiochemical and Biophysical Research Communications
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