Search results for "biological phenomena"

showing 10 items of 102 documents

p42 MAPK phosphorylates 80 kDa MARCKS at Ser-113.

1996

Abstract It is demonstrated here that p42 MAPKinase (p42 MAPK) phosphorylates the M yristoylated A lanine- R ich C - K inase S ubstrate (MARCKS) at Ser-113. In permeabilised Swiss 3T3 cells activation of protein kinase C (PKC) leads to p42 MAPK activation, but only the protein kinase C sites in MARCKS become phosphorylated and not Ser-113. The mitogen platelet-derived growth factor (PDGF) elicits the same response. These results demonstrate that while Ser-113 is a substrate for p42 MAPK in vitro and can be phosphorylated in vivo as shown by Taniguchi et al. [(1994) J. Biol. Chem. 269, 18299–18302], its phosphorylation is not subject to acute regulation by p42 MAPK in Swiss 3T3 cells.

MAPK/ERK pathwayMARCKSmedicine.medical_treatmentMitogen-activated protein kinase kinaseBiochemistryenvironment and public healthSubstrate SpecificityMiceStructural BiologySerinep42MAPKinasePhosphorylationMyristoylated Alanine-Rich C Kinase SubstrateCells CulturedProtein Kinase CMitogen-Activated Protein Kinase 1Platelet-Derived Growth FactorbiologyChemistryIntracellular Signaling Peptides and Proteins3T3 CellsProtein-Tyrosine KinasesCell biologyBiochemistryMitogen-activated protein kinasePhosphorylationTetradecanoylphorbol Acetatebiological phenomena cell phenomena and immunityPlatelet-derived growth factor receptorhormones hormone substitutes and hormone antagonistsendocrine systemRecombinant Fusion ProteinsMolecular Sequence DataBiophysicsGeneticsmedicineAnimalsAmino Acid SequenceMARCKSMolecular BiologyProtein kinase CGrowth factorMembrane ProteinsProteinsCell BiologyPeptide FragmentsEnzyme ActivationMolecular Weightenzymes and coenzymes (carbohydrates)Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMutagenesis Site-DirectedMitogensFEBS letters
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Use of CDC2 from etoposide-treated cells as substrate to assay CDC25 phosphatase activity

1999

International audience; Cyclin-dependent kinases (CDKs) regulate the key transition of the cell cycle in all organisms. In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Here we report that upon Etoposide treatment CDC2 is phosphorylated on tyrosine 15 and is dephosphorylated and activated in vitro by recombinant CDC25 phosphatase. We also show that inactive CDC2 kinase from Etoposide-treated cells can be used as a substrate in a sensitive two-step assay of CDC25 phosphatase. This assay, which is very simple to set-up, is based on the monitoring of CDC2 kinase activity after CDC25-depe…

MESH: HumansMESH: Phosphorylation[SDV]Life Sciences [q-bio]Cell Cycle Proteins[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]MESH: CDC2 Protein KinaseMESH: Tyrosine[SDV] Life Sciences [q-bio]AGENT ANTITUMORALenzymes and coenzymes (carbohydrates)MESH: Cell Cycle ProteinsMESH: cdc25 PhosphatasesCDC2 Protein KinaseMESH: HeLa CellsMESH: Phosphoprotein PhosphatasesPhosphoprotein PhosphatasesHumansTyrosinecdc25 PhosphatasesPhosphorylationbiological phenomena cell phenomena and immunityEtoposideHeLa CellsMESH: Etoposide
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Neural stem cell lineage-specific cannabinoid type-1 receptor regulates neurogenesis and plasticity in the adult mouse hippocampus

2018

Abstract Neural stem cells (NSCs) in the adult mouse hippocampus occur in a specific neurogenic niche, where a multitude of extracellular signaling molecules converges to regulate NSC proliferation as well as fate and functional integration. However, the underlying mechanisms how NSCs react to extrinsic signals and convert them to intracellular responses still remains elusive. NSCs contain a functional endocannabinoid system, including the cannabinoid type-1 receptor (CB1). To decipher whether CB1 regulates adult neurogenesis directly or indirectly in vivo, we performed NSC-specific conditional inactivation of CB1 by using triple-transgenic mice. Here, we show that lack of CB1 in NSCs is su…

Male0301 basic medicineCell signalingCannabinoid receptorNeurogenesisCognitive NeuroscienceLong-Term PotentiationMice Transgenicmouse hippocampus ; neural stem cells ; neurogenesis-dependent behavior ; CB1 ; adult neurogenesisHippocampal formationBiologyHippocampus03 medical and health sciencesCellular and Molecular Neurosciencemouse hippocampus0302 clinical medicineNeural Stem CellsReceptor Cannabinoid CB1Animalsreproductive and urinary physiologySpatial MemoryBehavior AnimalNeurogenesisLong-term potentiationOriginal ArticlesCB1Endocannabinoid systemneurogenesis-dependent behaviorNeural stem cellCell biologyadult neurogenesisMice Inbred C57BL030104 developmental biologynervous systemlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityStem cell030217 neurology & neurosurgeryCerebral Cortex
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Differential impact of high and low penetrance TNFRSF1A gene mutations on conventional and regulatory CD4+ T cell functions in TNFR1-associated perio…

2015

Abstract TNFR-associated periodic syndrome is an autoinflammatory disorder caused by autosomal-dominant mutations in TNFRSF1A, the gene encoding for TNFR superfamily 1A. The lack of knowledge in the field of TNFR-associated periodic syndrome biology is clear, particularly in the context of control of immune self-tolerance. We investigated how TNF-α/TNFR superfamily 1A signaling can affect T cell biology, focusing on conventional CD4+CD25− and regulatory CD4+CD25+ T cell functions in patients with TNFR-associated periodic syndrome carrying either high or low penetrance TNFRSF1A mutations. Specifically, we observed that in high penetrance TNFR-associated periodic syndrome, at the molecular le…

Male0301 basic medicinePenetranceAutoimmunitymedicine.disease_causeT-Lymphocytes RegulatoryImmune toleranceSettore MED/38 - Pediatria Generale E SpecialisticaTRAPS; Tconvs; Tregs; autoimmunity; immune toleranceImmunology and AllergyIL-2 receptorChildGeneticsMutationTconvTOR Serine-Threonine Kinaseshemic and immune systemsMiddle AgedAcquired immune systemPenetranceTregSTAT Transcription Factorsmedicine.anatomical_structureReceptors Tumor Necrosis Factor Type ICytokinesFemalebiological phenomena cell phenomena and immunitySignal TransductionAdultAdolescentFeverT cellAutoimmunity; Immune tolerance; Tconvs; Tregs; TRAPS; Cell Biology; ImmunologyImmunologyReceptors Antigen T-CellContext (language use)Tregs[object Object]BiologyImmunophenotypingYoung Adult03 medical and health sciencesImmune systemmedicineHumansAgedCell ProliferationDemographyTconvsImmune toleranceHereditary Autoinflammatory DiseasesTRAPSCell Biologybiological factors030104 developmental biologyMutationCancer research
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Gut microbiota steroid sexual dimorphism and its impact on gonadal steroids: influences of obesity and menopausal status

2020

[Background]: Gonadal steroid hormones have been suggested as the underlying mechanism responsible for the sexual dimorphism observed in metabolic diseases. Animal studies have also evidenced a causal role of the gut microbiome and metabolic health. However, the role of sexual dimorphism in the gut microbiota and the potential role of the microbiome in influencing sex steroid hormones and shaping sexually dimorphic susceptibility to disease have been largely overlooked. Although there is some evidence of sex-specific differences in the gut microbiota diversity, composition, and functionality, the results are inconsistent. Importantly, most of these studies have not taken into account the go…

Male:Health Care::Environment and Public Health::Public Health::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Cross-Sectional Studies [Medical Subject Headings]PhysiologyGut flora:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Mice:Chemicals and Drugs::Hormones Hormone Substitutes and Hormone Antagonists::Hormones::Gonadal Hormones [Medical Subject Headings]0302 clinical medicineOverweight persons:Organisms::Eukaryota::Animals [Medical Subject Headings]TestosteroneProgesteronaGonadal Steroid HormonesTestosteronaTestosteroneProgesterone:Persons::Persons::Age Groups::Adult::Aged [Medical Subject Headings]Sex Characteristics0303 health sciencesMicrobiotaIntestins -- MalaltiesMiddle AgedSex ; Gender ; Gonadal steroids ; Testosterone ; Progesterone ; Microbiome ; Sexual dimorphism.Persones obeses3. Good healthMenopause:Phenomena and Processes::Microbiological Phenomena::Microbiota [Medical Subject Headings]Intestins -- MicrobiologiaCaracteres sexualeslcsh:QR100-130Female:Phenomena and Processes::Reproductive and Urinary Physiological Phenomena::Reproductive Physiological Phenomena::Climacteric::Menopause [Medical Subject Headings]SexAnimal studiesIntestines -- DiseasesMenopauseMenopausaAdultMicrobiology (medical):Phenomena and Processes::Reproductive and Urinary Physiological Phenomena::Reproductive Physiological Phenomena::Sex Characteristics [Medical Subject Headings]:Check Tags::Male [Medical Subject Headings]SexoSteroid biosynthesisBiologyIntestines -- Microbiologydigestive systemMicrobiologylcsh:Microbial ecology:Health Care::Environment and Public Health::Public Health::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Case-Control Studies [Medical Subject Headings]03 medical and health sciencesSexual dimorphismmedicineAnimalsHumansObesityMicrobiome:Persons::Persons::Age Groups::Adult [Medical Subject Headings]Aged030304 developmental biology:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Mice [Medical Subject Headings]ResearchGender:Persons::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]medicine.diseasebiology.organism_classificationObesityGastrointestinal Microbiome:Diseases::Nutritional and Metabolic Diseases::Nutrition Disorders::Overnutrition::Obesity [Medical Subject Headings]Gonadal steroidsSexual dimorphismCross-Sectional Studies:Check Tags::Female [Medical Subject Headings]Case-Control StudiesIdentidad de géneroMicrobiome030217 neurology & neurosurgeryMicrobiome
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Analysis of methylation and mRNA expression status ofFADD andFAS genes in patients with oral squamous cell carcinoma

2014

Background: Apoptosis is an important mechanism that is responsible for the physiological deletion of harmful, damaged, or unwanted cells. Changed expression of apoptosis-related genes may lead to abnormal cell proliferation and finally to tumorigenesis. Our aims were to analyze the promoter methylation and gene expression profiles of FADD and FAS genes in risk of OSCC. Material and Methods: we analyze the promoter methylation status of FADD and FAS genes using Methylation - Specific PCR (MSP) in 86 OSCC tissues were kept in paraffin and 68 normal oral tissues applied as control. Also, FADD and FAS genes expression were analyzed in 19 cases and 20 normal specimens by Real-Time Reverse- Tran…

MaleMrna expressionFas-Associated Death Domain ProteinOdontologíamedicine.disease_causeurologic and male genital diseasesGene expressionmedicineHumansIn patientFADDRNA Messengerfas ReceptorGeneral DentistryGeneOral Medicine and PathologybiologyResearchMethylationDNA MethylationMiddle Aged:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludOtorhinolaryngologyApoptosisUNESCO::CIENCIAS MÉDICASbiology.proteinCancer researchCarcinoma Squamous CellSurgeryFemaleMouth Neoplasmsbiological phenomena cell phenomena and immunityCarcinogenesisMedicina Oral, Patología Oral y Cirugía Bucal
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Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain.

2018

The function of somatic stem cells declines with age. Understanding the molecular underpinnings of this decline is key to counteract age-related disease. Here, we report a dramatic drop in the neural stem cells (NSCs) number in the aging murine brain. We find that this smaller stem cell reservoir is protected from full depletion by an increase in quiescence that makes old NSCs more resistant to regenerate the injured brain. Once activated, however, young and old NSCs show similar proliferation and differentiation capacity. Single-cell transcriptomics of NSCs indicate that aging changes NSCs minimally. In the aging brain, niche-derived inflammatory signals and the Wnt antagonist sFRP5 induce…

MaleNeurogenesisSubventricular zoneInflammationBiologyGeneral Biochemistry Genetics and Molecular BiologyTranscriptome03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsmedicineAging brainsFRP5stem cell agingAnimalsHomeostasisquiescenceStem Cell Nichereproductive and urinary physiologyCellular Senescence030304 developmental biologyneural stem cellsCell Proliferation0303 health sciencesWnt signaling pathwayAge Factorssubventricular zoneBrainmodelingCell DifferentiationinterferonWnt signalingNeural stem cellCell biologynervous system diseasesNerve RegenerationMice Inbred C57BLmedicine.anatomical_structurenervous systeminflammationsimulationsmedicine.symptomStem cellbiological phenomena cell phenomena and immunitysingle-cell transcriptomics030217 neurology & neurosurgeryCell DivisionAdult stem cellCell
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Aurora-A Is Essential for the Tumorigenic Capacity and Chemoresistance of Colorectal Cancer Stem Cells

2010

Abstract Colorectal cancer stem cells (CR-CSC) are responsible for the generation and maintenance of intestinal tumors and are highly resistant to conventional chemotherapeutic agents. Aurora-A, a serine-threonine kinase involved in mitosis regulation, plays multiple key functions in tumor initiation and progression. We found that Aurora-A is overexpressed in primary colorectal tumor cells, in the CR-CSC fraction, and in stem cell–derived differentiated cells, compared with normal colon tissue. Aurora-A expression was functionally linked to centrosome amplification in CR-CSC, as indicated by the decrease in cells with multiple centrosomes that followed Aurora-A silencing. Knockdown of Auror…

MaleOncologyCancer Researchmedicine.medical_specialtyColorectal cancerCellular differentiationcolorectal cancer stem cellsMice NudeCell Growth ProcessesTumor initiationProtein Serine-Threonine KinasesBiologyMiceAurora KinasesCell MovementCancer stem cellInternal medicinemedicineAnimalsHumansCytotoxic T cellGene silencingMitosisAgedAurora Kinase ACentrosomeCell CycleGene AmplificationMiddle Agedmedicine.diseaseOncologyDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsCancer researchFemalebiological phenomena cell phenomena and immunityStem cellColorectal NeoplasmsCancer Research
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The clinical significance of CDK1 expression in oral squamous cell carcinoma

2014

Objectives: To evaluate the clinical significance of cyclin-dependent kinase 1 (CDK 1 ) in 77 oral squamous cell carcinomas (OSCC) using immunohistochemical methods. Study Design: Immunohistochemical expression of CDK 1 was compared with various clinicopathological features in 77 OSCC and 60 controlled epithelia adjacent to the tumours. In addition, correlation of CDK 1 expression and prognostic and the 5-year accumulative survival rate of OSCC were investigated. Results: The CDK 1 protein was expressed in 52 cases of 77 tumor tissues (67.5%), compared with 21 cases of 60 controlled (35.0%). The expression of CDK 1 was significantly correlated with the histological grade of OSCC ( P <0.05).…

MalePathologymedicine.medical_specialtyCellOdontologíaenvironment and public healthCDC2 Protein KinaseHumansMedicineClinical significanceGeneral DentistrySurvival rateMouth neoplasmCyclin-dependent kinase 1Oral Medicine and Pathologybusiness.industryKinaseCell growthResearchMiddle Aged:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludImmunohistochemistrySurvival Rateenzymes and coenzymes (carbohydrates)stomatognathic diseasesmedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASCarcinoma Squamous CellCancer researchImmunohistochemistryFemaleMouth NeoplasmsSurgerybiological phenomena cell phenomena and immunitybusinessMedicina Oral Patología Oral y Cirugia Bucal
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Accumulation of hydroxyethyl starch (HES) in the liver of patients with renal failure and portal hypertension

1986

Summary Hydroxyethyl starch (HES) has gained wide clinical acceptance as a colloidal plasma substitute. We were able to study the liver biopsies of two patients with renal failure who developed ascites after repeated infusions of HES. All types of liver cells displayed massive accumulation of HES with the morphologic resemblance to a storage disease. These changes could be distinguished clearly from the lesions of a hereditary disorder by light and electron microscopy. Although it is difficult to establish a causative role for HES in the development of ascites on the bases of morphological changes alone, one should be cautious about giving HES to patients with renal failure until exact data…

Malemedicine.medical_specialtyResuscitationPathologyHydroxyethyl starchHydroxyethyl Starch DerivativesRenal DialysisHypertension PortalAscitesmedicineHumansreproductive and urinary physiologyHepatologybusiness.industryStarchMiddle Agedmedicine.diseaseSurgeryMicroscopy ElectronLiverKidney Failure ChronicPortal hypertensionFemaleHypotensionbiological phenomena cell phenomena and immunitymedicine.symptombusinessPerfusionmedicine.drugJournal of Hepatology
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