Search results for "Suppressor"

showing 10 items of 532 documents

Functional Assessment of Variants in the TSC1 and TSC2 Genes Identified in Individuals with Tuberous Sclerosis Complex

2011

The effects of missense changes and small in-frame deletions and insertions on protein function are not easy to predict, and the identification of such variants in individuals at risk of a genetic disease can complicate genetic counselling. One option is to perform functional tests to assess whether the variants affect protein function. We have used this strategy to characterize variants identified in the TSC1 and TSC2 genes in individuals with, or suspected of having, Tuberous Sclerosis Complex (TSC). Here we present an overview of our functional studies on 45 TSC1 and 107 TSC2 variants. Using a standardized protocol we classified 16 TSC1 variants and 70 TSC2 variants as pathogenic. In add…

congenital hereditary and neonatal diseases and abnormalitiesGenetic counselingtuberous sclerosis complexBiologyTuberous Sclerosis Complex 1 Protein03 medical and health sciencesTuberous sclerosis0302 clinical medicineTuberous SclerosisGenetic variationTuberous Sclerosis Complex 2 ProteinGeneticsmedicineMissense mutationHumansunclassified variantsGeneGenetics (clinical)Cells Cultured030304 developmental biologyGenetics0303 health sciencesModels GeneticTumor Suppressor ProteinsLife SciencesGenetic Variationmedicine.diseaseTSC23. Good healthnervous system diseasesTSC1medicine.anatomical_structureTSC1TSC2030217 neurology & neurosurgeryCommon disease-common variant
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RASSF1A inhibits estrogen receptor alpha expression and estrogen-independent signalling: implications for breast cancer development

2012

The Ras association domain family 1 isoform A (RASSF1A) is a tumor suppressor whose inactivation is implicated in the development of many human cancers, including breast carcinomas. Little is known about the tumor-suppressive function of RASSF1A in breast tissue and whether its inactivation is mechanistically involved in the initiation and progression of breast tumors. Here, we show that RASSF1A inhibits breast cancer growth in vivo, and suppresses estrogen receptor (ERα) expression and function. Reconstitution of RASSF1A in MCF7 cells led to decreased ERα levels and reduced sensitivity to estrogen (E2). Concomitantly, we observed decreased expression of Id1 as well as the E2-responsive gen…

endocrine systemCancer Researchmedicine.medical_specialtyCell SurvivalGene ExpressionEstrogen receptorApoptosisBreast NeoplasmsCell Cycle ProteinsMice SCIDBiologyMiceBreast cancerDownregulation and upregulationMice Inbred NODInternal medicineGeneticsmedicineAnimalsHumansFulvestrantMolecular BiologyCellular SenescenceCell ProliferationRegulation of gene expressionEstradiolFulvestrantTumor Suppressor ProteinsEstrogen AntagonistsEstrogen Receptor alphaCancerEstrogensCell Cycle Checkpointsmedicine.diseaseGene Expression Regulation NeoplasticEndocrinologyProteolysisMCF-7 CellsCancer researchFemaleEctopic expressionEstrogen receptor alphaNeoplasm TransplantationSignal Transductionmedicine.drugOncogene
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1H, 13C and 15N NMR chemical shift assignments of cAMP-regulated phosphoprotein-19 and -16 (ARPP-19 and ARPP-16)

2020

Protein Phosphatase 2A, PP2A, the principal Serine/threonine phosphatase, has major roles in broad range of signaling pathways that include regulation of cell cycle, cell proliferation and neuronal signaling. The loss of function of PP2A is linked with many human diseases, like cancer and neurodegenerative disorders. Protein phosphatase 2A (PP2A) functions as tumor suppressor and its tumor suppressor activity is inhibited by the overexpression of PP2A inhibitor proteins in most of the cancers. ARPP-19/ARPP-16 has been identified as one of the potential PP2A inhibitor proteins. Here, we report the resonance assignment of backbone 1H, 13C and 15N atoms of human ARPP-19 and ARPP-16 proteins. T…

entsyymitcAMP-regulated phosphoprotein-19HA-detection intrinsically disordered proteinBiochemistryArticlelaw.inventionSerine03 medical and health sciencesNMR spectroscopy0302 clinical medicineStructural BiologylawAssignmentsNMR-spektroskopiaLoss function030304 developmental biologysoluviestintä0303 health sciencesCell growthChemistryassignmentsProtein phosphatase 2Nuclear magnetic resonance spectroscopyCell cycle3. Good healthCell biologySuppressorproteiinitSignal transduction030217 neurology & neurosurgeryBiomolecular NMR Assignments
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Progenitor death drives retinal dysplasia and neuronal degeneration in a mouse model of Atrip-Seckel syndrome

2020

ABSTRACT Seckel syndrome is a type of microcephalic primordial dwarfism (MPD) that is characterized by growth retardation and neurodevelopmental defects, including reports of retinopathy. Mutations in key mediators of the replication stress response, the mutually dependent partners ATR and ATRIP, are among the known causes of Seckel syndrome. However, it remains unclear how their deficiency disrupts the development and function of the central nervous system (CNS). Here, we investigated the cellular and molecular consequences of ATRIP deficiency in different cell populations of the developing murine neural retina. We discovered that conditional inactivation of Atrip in photoreceptor neurons …

lcsh:MedicineMedicine (miscellaneous)315BlindnessMicechemistry.chemical_compoundImmunology and Microbiology (miscellaneous)Cell DeathneurodevelopmentStem CellsNeurodegenerationapoptosisneurodegenerationSyndromeCell biologyDNA-Binding Proteinsdna damage responsemedicine.anatomical_structurePhotoreceptor Cells VertebrateResearch Articlelcsh:RB1-214NeurogenesisNeuroscience (miscellaneous)Embryonic DevelopmentBiologyRetinaGeneral Biochemistry Genetics and Molecular Biologylcsh:PathologymedicineAnimalsAbnormalities MultipleProgenitor cellVision OcularAdaptor Proteins Signal TransducingCell ProliferationProgenitorRetinalcsh:RRetinalEmbryo Mammalianmedicine.diseasephotoreceptorDisease Models AnimalSeckel syndromechemistryvisual system developmentNerve DegenerationRetinal dysplasiaRetinal DysplasiaTumor Suppressor Protein p53Primordial dwarfismDNA DamageDisease Models & Mechanisms
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Suppression and mediation effect in psychosocial intervention: differences, similarities and examples

2013

El presente trabajo compara el efecto mediador y el supresor de una tercera variable. Ambos efectos parcelan la varianza de la variable dependiente (Y). La mediación es la reducción, tras introducir una tercera variable (Z) en el modelo, de la proporción de varianza explicada directamente por la variable independiente (X) en la variable criterio (Y) y la supresión es el incremento de la proporción de varianza explicada directamente por la independiente en la variable criterio, al incluir la tercera variable en el modelo. Se analizan las características y diferencias de cada efecto y se examina en qué situaciones se produce uno u otro. Cada situación, compuesta de tres variables correlaciona…

lcsh:PsychologyTerceras variablesPsychosocial researchlcsh:BF1-990Intervención psicosocialInvestigación psicosocialPsychosocial interventionSuppressor effectMediaciónSupresiónThird variablesMediator effect
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Current advancement in immunosensing of p53 tumor suppressor protein based on nanomaterials: Analytical approach

2017

Abstract The utility of detection of p53 in tomorrow's personalized health care field will mean early and accurate diagnosis of many types of cancers. This review is meant to provide an overview of the various types of immunosensors and immunoassay have been developed for determination of p53, along with significant advances over the last several years in related technologies. In addition, this review described: • Most frequently applied principles in immunoassay/immunosensing of p53. • The aspects of fabrication in the perspective of immunoassay/immunosensing applications. • The potential of various electrochemical, electrochemiluminescence immunosensors for the determination of p53 within…

medicine.diagnostic_testComputer science010401 analytical chemistryNanotechnologyPersonalized health02 engineering and technology021001 nanoscience & nanotechnology01 natural sciences0104 chemical sciencesAnalytical ChemistryTumor BiomarkersImmunoassayP53 Tumor Suppressor ProteinmedicineElectrochemiluminescence0210 nano-technologySpectroscopyTrAC Trends in Analytical Chemistry
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Identification and characterization of a monoclonal antibody to the membrane fatty acid binding protein

1992

A monoclonal antibody to the rat liver membrane fatty acid binding protein (MFABP) was prepared by immunizing mice with purified MFABP isolated from solubilized rat liver plasma membrane proteins by oleate-agarose affinity chromatography technique. The monoclonal antibody K15/6 identified a single 40 kDa protein in rat liver plasma membranes with pI values of 8.5, 8.8 and 9.0, which is identical to the authentic MFABP, but clearly distinct from rat mitochondrial GOT. The antibody K15/6 selectively inhibited cellular influx as well as membrane binding of fatty acids, but not of cholesterol or vitamin E. The same antibody was used in immunofluorescence, ELISA and Western blot analysis to dete…

medicine.drug_classBlotting WesternImmunoblottingBiophysicsFluorescent Antibody TechniqueEnzyme-Linked Immunosorbent AssayNerve Tissue ProteinsFatty Acid-Binding ProteinsMonoclonal antibodyBiochemistryFatty acid-binding proteinCell LineMiceEndocrinologyAffinity chromatographymedicineAnimalsHumanschemistry.chemical_classificationMice Inbred BALB CbiologyMembrane transport proteinTumor Suppressor ProteinsBinding proteinCell MembraneFatty AcidsAntibodies MonoclonalFatty acidMolecular biologyNeoplasm ProteinsRatsLiverchemistryMembrane proteinBiochemistrybiology.proteinElectrophoresis Polyacrylamide GelAntibodyCarrier ProteinsFatty Acid-Binding Protein 7Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism
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Synergistic cytotoxic interactions between sodium butyrate, MG132 and camptothecin in human retinoblastoma Y79 cells.

2000

This paper studies the effects caused in human retinoblastoma Y79 cells by treatment with combinations of sodium butyrate, the inhibitor of topoisomerase I camptothecin and the inhibitor of 26S proteasome MG132. The combination of sodium butyrate and camptothecin resulted in a strong synergistic cytotoxicity, as revealed by combination indices of 0.77 and 0.52 calculated at IC(50) and IC(75). Synergistic interactions were also demonstrated for combinations of sodium butyrate and MG132, camptothecin and MG132 and for a combination of all three compounds. The cytotoxic effects observed after the combined treatments can be considered a consequence of apoptosis, as suggested by the appearance o…

medicine.drug_classCell SurvivalLeupeptinsSodiumchemistry.chemical_elementApoptosisButyrateBiologyCysteine Proteinase Inhibitorschemistry.chemical_compoundMG132Antineoplastic Combined Chemotherapy ProtocolsmedicineTumor Cells CulturedHumansheterocyclic compoundsEnzyme InhibitorsRetinoblastomaCaspase 3TopoisomeraseRetinoblastomaSodium butyrateDrug SynergismGeneral Medicinemedicine.diseaseeye diseasesEnzyme ActivationButyrateschemistryBiochemistryProto-Oncogene Proteins c-bcl-2CaspasesCancer researchbiology.proteinCamptothecinTopoisomerase I InhibitorsTumor Suppressor Protein p53CamptothecinTopoisomerase inhibitormedicine.drugTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
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General considerations in the interpretation of I-J genetic restrictions: evidence that the antigen-binding chain of antigen-specific T-suppressor fa…

1987

SUMMARY (CBA × B10)F1 [(H-2k x H-2b)] mice produce two types of antigen-specific T-suppressor factor (TsF), which can be separated by affinity chromatography on anti-I-J monoclonal antibody. After reduction and alkylation, both chains of F1 TsF are required for biological activity. However, the antigen-binding chain (AgBC) of F1 TsFk (AgBCk) is only complemented by I-Jk and likewise for F1 TsFb. In other words, interchain complementation shows the same genetic restriction in interchain complementation in parental and F1 mice. F1 TsF bearing, for example, I-Jk (TsFk), interacts with haptenized ‘antigen-presenting cells’ (‘APC’) of both parental haplotypes, and may be described as showing dua…

medicine.drug_classImmunologyAntigen-Presenting CellsImmunogeneticsBiologyMonoclonal antibodyModels BiologicalEpitopesMiceStructure-Activity RelationshipAntigenAffinity chromatographySpecies SpecificityGeneticsmedicineSuppressor Factors ImmunologicAnimalsBinding siteReceptorCrosses GeneticGeneticsBinding SitesHaplotypeGenetic Complementation TestHistocompatibility Antigens Class IIComplementationHaplotypesJournal of immunogenetics
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Novel missense mutation of the TP63 gene in a newborn with Hay-Wells/Ankyloblepharon-Ectodermal defects-Cleft lip/palate (AEC) syndrome: clinical rep…

2021

Abstract Introduction Ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) syndrome, also known as Hay-Wells syndrome, is a rare genetic syndrome with ectodermal dysplasia. About 100 patients have been reported to date. It is associated to a heterozygous mutation of the tumor protein p63 (TP63) gene, located on chromosome 3q28. Typical clinical manifestations include: filiform ankyloblepharon adnatum (congenital adherence of the eyelids), ectodermal abnormalities (sparse and frizzy hair, skin defects, nail alterations, dental changes and hypohidrosis), and cleft lip/palate. Diagnostic suspicion is based on clinical signs and confirmed by genetic testing. Patient’s presentation We hereb…

medicine.medical_specialtyEctodermal dysplasiaHay–Wells syndromeCleft LipAnkyloblepharonMutation MissenseErythrodermaCase ReportEctodermal dysplasiaPediatricsRJ1-570TP63medicineMissense mutationHumansEye Abnormalitiesbusiness.industryTumor Suppressor ProteinsAEC syndromeInfant NewbornTumor protein p63 geneEyelidsmedicine.diseaseAnkyloblepharon-ectodermal defects-cleft lip/palate syndromeDermatologyCleft Palatemedicine.anatomical_structureHay-Wells syndromeScalpAgenesisFemaleAEC syndrome Ankyloblepharon-ectodermal defects-cleft lip/palate syndrome Congenital skin disorders Ectodermal dysplasia Hay-Wells syndrome Tumor protein p63 genebusinessTranscription FactorsCongenital skin disordersItalian journal of pediatrics
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