Search results for "BINDING PROTEIN"

showing 10 items of 1292 documents

A girl with an atypical form of ataxia telangiectasia and an additional de novo 3.14Mb microduplication in region 19q12

2011

A 9-year-old girl born to healthy parents showed manifestations suggestive of ataxia telangiectasia (AT), such as short stature, sudden short bouts of horizontal and rotary nystagmus, a weak and dysarthric voice, rolling gait, unstable posture, and atactic movements. She did not show several cardinal features typical of AT such as frequent, severe infections of the respiratory tract. In contrast, she showed symptoms not generally related to AT, including microcephaly, profound motor and mental retardation, small hands and feet, severely and progressively reduced muscle tone with slackly protruding abdomen and undue drooling, excess fat on her upper arms, and severe oligoarthritis. A cranial…

medicine.medical_specialtyMicrocephalyPathologyCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesBiologyShort statureAtaxia Telangiectasia Mutated ProteinsAtaxia TelangiectasiaInternal medicineChromosome DuplicationGene duplicationGeneticsmedicineHumansLymphocytesChildSalivaCerebellar hypoplasiaMetaphaseGenetics (clinical)Mental DisordersTumor Suppressor ProteinsGeneral Medicinemedicine.diseaseDNA-Binding ProteinsEndocrinologyChromosome InversionAtaxia-telangiectasiaChromosomal regionSpeech delayMicrocephalyFemalemedicine.symptomApoptosis Regulatory ProteinsChromosomes Human Pair 19DNA DamageEuropean Journal of Medical Genetics
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PGC-1α: a master gene that is hard to master

2012

Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) is a transcriptional coactivator that favorably affects mitochondrial function. This concept is supported by an increasing amount of data including studies in PGC-1α gene-deleted mice, suggesting that PGC-1α is a rescue factor capable of boosting cell metabolism and promoting cell survival. However, this view has now been called into question by a recent study showing that adeno-associated virus-mediated PGC-1α overexpression causes overt cell degeneration in dopaminergic neurons. How is this to be understood, and can these seemingly conflicting findings tell us something about the role of PGC-1α in cell stress and in cont…

medicine.medical_specialtyModels NeurologicalSettore BIO/11 - Biologia MolecolareRNA-binding proteinBiologyMitochondrionSettore BIO/09 - FisiologiaMiceCellular and Molecular NeuroscienceHeat shock proteinInternal medicinemedicineAnimalsHomeostasisHumansReceptorMolecular BiologyTranscription factorHeat-Shock ProteinsMice KnockoutPharmacologyPGC-1α Mitochondria Dopaminergic neurons Transgenic animal Adenovirus Parkinson’s diseaseDopaminergic NeuronsDopaminergicRNA-Binding ProteinsParkinson DiseaseCell BiologyPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaEndocrinologyCell metabolismNerve DegenerationTrans-ActivatorsMolecular MedicineNeuroscienceHomeostasisTranscription FactorsCellular and Molecular Life Sciences
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Can you blame cold feet on Epac (and Rap1A)? Focus on “Cyclic AMP-Rap1A signaling activates RhoA to induce α2C-adrenoceptor translocation to the cell…

2012

Intracellular signaling by the second messenger cyclic AMP (cAMP) activates the Ras-related small GTPase Rap1 through the guanine exchange factor Epac. This activation leads to effector protein interactions, activation, and biological responses in the vasculature, including vasorelaxation. In vascular smooth muscle cells derived from human dermal arterioles (microVSM), Rap1 selectively regulates expression of G protein-coupled α2C-adrenoceptors (α2C-ARs) through JNK-c-jun nuclear signaling. The α2C-ARs are generally retained in the trans-Golgi compartment and mobilize to the cell surface and elicit vasoconstriction in response to cellular stress. The present study used human microVSM to exa…

medicine.medical_specialtyRHOAPhysiologyMyocytes Smooth MuscleCellChromosomal translocationSmooth muscleReceptors Adrenergic alpha-2Internal medicineCyclic AMPmedicineAnimalsHumansReceptorbiologyrap1 GTP-Binding ProteinsArticlesCell Biologyα2c adrenoceptorCell biologyProtein Transportmedicine.anatomical_structureEndocrinologybiology.proteinmedicine.symptomrhoA GTP-Binding ProteinVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Regulation of the human bradykinin B2 receptor expressed in sf21 insect cells: A possible role for tyrosine kinases

2000

The functional regulation of the human bradykinin B2 receptor expressed in sf21 cells was studied. Human bradykinin B2 receptors were immunodetected as a band of 75–80 kDa in membranes from recombinant baculovirus-infected cells and visualized at the plasma membrane, by confocal microscopy, using an antibody against an epitope from its second extracellular loop. B2 receptors, detected in membranes by [3H-bradykinin] binding, showed a Kd of 0.66 nmol/L and an expression level of 2.57 pmol/mg of protein at 54 h postinfection. In these cells, bradykinin induced a transient increase of intracellular calcium ([Ca2+]i) in fura 2-AM loaded sf21 cells, and promoted [35S]-GTPγS binding to membranes.…

medicine.medical_specialtyReceptor Bradykinin B2G proteinGene Expressionchemistry.chemical_elementBradykininReceptors Cell SurfaceSpodopteraCalciumBiologyBradykininBiochemistryCalcium in biologychemistry.chemical_compoundGTP-Binding ProteinsInternal medicineHomologous desensitizationmedicineAnimalsHumansPhosphorylationBradykinin receptorPhosphoamino AcidsReceptorOctopamineMolecular BiologyBradykinin Receptor AntagonistsCells CulturedMicroscopy ConfocalReceptors BradykininCell MembraneCell BiologyProtein-Tyrosine KinasesTyrphostinsGenisteinMolecular biologyRecombinant ProteinsEndocrinologychemistryGuanosine 5'-O-(3-Thiotriphosphate)ThapsigarginCalciumBaculoviridaeTyrosine kinaseProtein BindingJournal of Cellular Biochemistry
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Retinoids induce MMP-9 expression through RARalpha during mammary gland remodeling.

2007

Retinoic acid (RA) is a signaling molecule in the morphogenesis of the mammary gland, modulating the expression of matrix metalloproteinases (MMPs). The aim of this paper was to study the role of RA during weaning, which consists of three events: apoptosis of the secretory cells, degradation of the extracellular matrix, and adipogenesis. CRABP II and CRBP-1 carrier proteins increased significantly during weaning compared with lactating glands but reverted to control values after the litter resuckled. The effects of RA are mediated by the nuclear receptors RARalpha, RARbeta, RARgamma, and RXRalpha, which underwent an increase in protein levels during weaning. In an attempt to elucidate the R…

medicine.medical_specialtyRetinyl EstersTime FactorsPhysiologymedicine.drug_classReceptors Retinoic AcidEndocrinology Diabetes and MetabolismMammary glandMorphogenesisRetinoic acidApoptosisTretinoinWeaningMatrix metalloproteinaseBiologyStromelysin 1chemistry.chemical_compoundRetinoidsMammary Glands AnimalPregnancyPhysiology (medical)Internal medicinemedicineAnimalsLactationInvolution (medicine)RetinoidRNA MessengerRats WistarVitamin AMammary gland involutionAdipogenesisRetinoic Acid Receptor alphaRetinol-Binding Proteins CellularMatrix MetalloproteinasesExtracellular MatrixRatsRetinol-Binding Proteinsmedicine.anatomical_structureEndocrinologychemistryMatrix Metalloproteinase 9Matrix Metalloproteinase 2FemaleDiterpenesSignal TransductionAmerican journal of physiology. Endocrinology and metabolism
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Thyroid hormones induce sumoylation of the cold shock domain-containing protein PIPPin in developing rat brain and in cultured neurons.

2006

We previously identified a cold shock domain (CSD)-containing protein (PIPPin), expressed at high level in brain cells. PIPPin has the potential to undergo different post-translational modifications and might be a good candidate to regulate the synthesis of specific proteins in response to extracellular stimuli. Here we report the effects of thyroid hormone (T3) on PIPPin expression in developing rat brain. We found that a significant difference among euthyroid- and hypothyroid- newborn rats concerns sumoylation of nuclear PIPPin, that is abolished by hypothyroidism. Moreover, T3-dependence of PIPPin sumoylation has been confirmed in cortical neurons purified from brain cortices and culture…

medicine.medical_specialtySUMO-1 ProteinSUMO proteinDeveloping rat brainNerve Tissue ProteinsEndocrinologyAntithyroid AgentsHypothyroidismPregnancyInternal medicinemedicineExtracellularAnimalsRats WistarCells CulturedCell NucleusCerebral CortexNeuronsbiologyRNA-Binding ProteinsCold-shock domainChromatinProtein Structure TertiaryRatsThyroid hormoneChemically defined mediumCell nucleusmedicine.anatomical_structureHistoneEndocrinologyAnimals NewbornPropylthiouracilPrenatal Exposure Delayed Effectsbiology.proteinTriiodothyronineRNA-binding proteins (RBPs)FemaleRabbitsNucleusEndocrinology
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Retarded thymic involution and massive germinal center formation in NF-ATp-deficient mice.

1998

NF-ATp and NF-ATc are the most prominent nuclear NF-AT transcription factors in peripheral T lymphocytes. After T cell activation both factors bind to and control the promoters and enhancers of numerous lymphokine and receptor ligand genes. In order to define a specific role for NF-ATp in vivo we have inactivated the NF-ATp gene by gene targeting in mice. We show that NF-ATp deficiency leads to the accumulation of peripheral T cells with a “preactivated” phenotype, enhanced immune responses of T cells after secondary stimulation in vitro and severe defects in the proper termination of antigen responses, as shown by a reduced deletion of superantigen-reactive CD4+ T cells. These alterations …

medicine.medical_specialtyT cellT-LymphocytesImmunologyApoptosisThymus GlandBiologyPolymerase Chain ReactionMiceImmune systemAntigenInternal medicinemedicineImmunology and AllergyCytotoxic T cellAnimalsfas ReceptorDNA PrimersMice KnockoutThymic involutionSuperantigensBase SequenceNFATC Transcription FactorsLymphokineGerminal centerNuclear ProteinsGerminal CenterMolecular biologyDNA-Binding ProteinsEndocrinologymedicine.anatomical_structureLymphatic systemPhenotypeTranscription FactorsEuropean journal of immunology
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Corticotropin-Releasing Hormone-Mediated Induction of Intracellular Signaling Pathways and Brain-Derived Neurotrophic Factor Expression Is Inhibited …

2005

CRH receptor (CRHR) 1 and the cannabinoid receptor 1 (CB1) are both G protein-coupled receptors. Activation of CRHR1 leadstoincreasesincAMPproductionandphosphorylationof the transcription factor cAMP response element-binding protein (CREB). In contrast, CB1 is negatively coupled to the cAMP signaling cascade. In this study, we analyzed a putative interaction between these two systems focusing on the regulation of the expression of brain-derived neurotrophic factor (BDNF), a CREB-regulated gene. In situ hybridization revealed coexpression of CRHR1 and CB1 receptors in the granular layer of the cerebellum. Therefore, we analyzed the effects of CRH and the CB1 agonist WIN-55,212-2 on BDNF expr…

medicine.medical_specialtyTime FactorsCorticotropin-Releasing HormoneMorpholinesmedicine.medical_treatmentImmunoblottingEnzyme-Linked Immunosorbent AssayTropomyosin receptor kinase BNaphthalenesCREBModels BiologicalRats Sprague-DawleyMiceEndocrinologyNeurotrophic factorsCerebellumInternal medicineCannabinoid Receptor ModulatorsCyclic AMPmedicineAnimalsRNA MessengerCyclic AMP Response Element-Binding ProteinReceptorEgtazic AcidCells CulturedIn Situ HybridizationNeuronsBrain-derived neurotrophic factorSulfonamidesbiologyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorCalcium Channel BlockersIsoquinolinesEndocannabinoid systemBenzoxazinesRatsMice Inbred C57BLPyrimidinesEndocrinologynervous systembiology.proteinCalciumCannabinoidSignal transductionEndocannabinoidsProtein BindingSignal TransductionEndocrinology
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A common mechanism of action of the selective serotonin reuptake inhibitors citalopram and fluoxetine: Reversal of chronic psychosocial stress-induce…

2010

The transcription factor CREB regulates adaptive responses like memory consolidation, addiction, and synaptic refinement. Recently, chronic psychosocial stress as animal model of depression has been shown to stimulate CREB transcriptional activity in the brain; this stimulation was prevented by treatment with the antidepressant imipramine, which inhibits both noradrenaline and serotonin reuptake. However, it was unknown whether the selective inhibition of serotonin reuptake is sufficient for inhibition of stress-induced CREB activation, as it is for the clinical antidepressant effect. Therefore, the effect of two selective serotonin reuptake inhibitors (SSRIs), citalopram and fluoxetine, wa…

medicine.medical_specialtyTranscription GeneticMice TransgenicCitalopramBiologyCitalopramCREBImipramineDrug Administration ScheduleMice03 medical and health sciences0302 clinical medicineGenes ReporterCREB in cognitionFluoxetineInternal medicinemedicineAnimalsPhosphorylationCyclic AMP Response Element-Binding ProteinTranscription factor030304 developmental biologyPharmacology0303 health sciencesFluoxetineBrain3. Good healthEndocrinologyGene Expression RegulationMechanism of actionbiology.proteinAntidepressantmedicine.symptomSelective Serotonin Reuptake InhibitorsStress Psychological030217 neurology & neurosurgerymedicine.drugEuropean Journal of Pharmacology
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p53 Involvement in the control of murine hair follicle regression.

2001

p53 is a transcription factor mediating a variety of biological responses including apoptotic cell death. p53 was recently shown to control apoptosis in the hair follicle induced by ionizing radiation and chemotherapy, but its role in the apoptosis-driven physiological hair follicle regression (catagen) remains to be elucidated. Here, we show that p53 protein is strongly expressed and co-localized with apoptotic markers in the regressing hair follicle compartments during catagen. In contrast to wild-type mice, p53 knockout mice show significant retardation of catagen accompanied by significant decrease in the number of apoptotic cells in the hair matrix. Furthermore, p53 null hair follicles…

medicine.medical_specialtyTumor suppressor genemedicine.medical_treatmentDown-RegulationApoptosisBiologyPathology and Forensic MedicineTelogen effluviumMiceBcl-2-associated X proteinDownregulation and upregulationInternal medicineProto-Oncogene ProteinsmedicineAnimalsbcl-2-Associated X ProteinMice Knockoutintegumentary systemGrowth factorAlopecia areatamedicine.diseaseHair follicleCell biologyUp-RegulationMice Inbred C57BLEndocrinologymedicine.anatomical_structureInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-bcl-2Knockout mousebiology.proteinCommentaryFemaleTumor Suppressor Protein p53Hair FollicleThe American journal of pathology
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