Search results for "Transporters"

showing 10 items of 203 documents

Identification and expansion of human osteosarcoma-cancer-stem cells by long-term 3-aminobenzamide treatment

2009

A novel cancer stem-like cell line (3AB-OS), expressing a number of pluripotent stem cell markers, was irreversibly selected from human osteosarcoma MG-63 cells by long-term treatment (100 days) with 3-aminobenzamide (3AB). 3AB-OS cells are a heterogeneous and stable cell population composed by three types of fibroblastoid cells, spindle-shaped, polygonal-shaped, and rounded-shaped. With respect to MG-63 cells, 3AB-OS cells are extremely smaller, possess a much greater capacity to form spheres, a stronger self-renewal ability and much higher levels of cell cycle markers which account for G1-S/G2-M phases progression. Differently from MG-63 cells, 3AB-OS cells can be reseeded unlimitedly wit…

AdultHomeobox protein NANOGAdolescentPhysiologyCellular differentiationClinical BiochemistryApoptosisBiologyStem cell markerYoung Adultcancer stemm cells osteosarcoma PARP inhibitorsCancer stem cellCell Line TumorSettore BIO/10 - BiochimicaHumansRhodamine 123Enzyme InhibitorsProgenitor cellChildInduced pluripotent stem cellCell ShapeCell potencyFluorescent DyesOsteosarcomaCell DifferentiationCell BiologyCalcium Channel BlockersDrug Resistance MultipleGene Expression Regulation NeoplasticVerapamilBenzamidesImmunologyNeoplastic Stem CellsCancer researchATP-Binding Cassette TransportersBenzimidazolesStem cellBiomarkersJournal of Cellular Physiology
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Dietary polyunsaturated fatty acids may increase plasma LDL-cholesterol and plasma cholesterol concentrations in carriers of an ABCG1 gene single nuc…

2011

Abstract Background ABCG1 mediates cellular cholesterol transport, but there is very little known about the influence of ABCG1 polymorphisms on human plasma lipoprotein cholesterol concentrations or on the interactions of these polymorphisms with diet. Objective Our objective was to investigate whether interactions between PUFA intake and ABCG1 polymorphisms modulate associations with plasma total cholesterol (TC), LDL- and HDL-cholesterol in two Spanish populations. Methods We grounded our investigation on two general population-based studies: the Hortega study (population A) and the Pizarra study (population B). Participants included 1178 individuals (50.0% women, age range 21–85 years) a…

AdultMaleHeterozygotemedicine.medical_specialtyPopulationSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideYoung Adultchemistry.chemical_compoundGene FrequencySurveys and QuestionnairesInternal medicineGenotypemedicineHumansGene–environment interactionAlleleeducationAllele frequencyATP Binding Cassette Transporter Subfamily G Member 1AgedAged 80 and overchemistry.chemical_classificationGeneticseducation.field_of_studyChi-Square DistributionCholesterolHomozygoteCholesterol LDLMiddle AgedDietUp-RegulationCholesterolPhenotypeEndocrinologychemistrySpainFatty Acids UnsaturatedATP-Binding Cassette TransportersFemaleGene-Environment Interactionlipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicinePolyunsaturated fatty acidAtherosclerosis
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Association Study of Nonsynonymous Single Nucleotide Polymorphisms in Schizophrenia

2010

Genome-wide association studies using several hundred thousand anonymous markers present limited statistical power. Alternatively, association studies restricted to common nonsynonymous single nucleotide polymorphisms (nsSNPs) have the advantage of strongly reducing the multiple testing problem, while increasing the probability of testing functional single nucleotide polymorphisms (SNPs).We performed a case-control association study of common nsSNPs in Galician (northwest Spain) samples using the Affymetrix GeneChip Human 20k cSNP Kit, followed by a replication study of the more promising results. After quality control procedures, the discovery sample consisted of 5100 nsSNPs at minor allel…

AdultMaleNonsynonymous substitutionGenotype"psychosis"methods [Genetic Association Studies]"mental brain homeostasis"Single-nucleotide polymorphismBiologygenetics [Cation Transport Proteins]Polymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineHumansGenetic Predisposition to Diseasegenetics [Schizophrenia]ddc:610statistics & numerical data [Genetic Association Studies]genetics [Genetic Predisposition to Disease]Cation Transport ProteinsGenetic Association StudiesBiological PsychiatryAged030304 developmental biology"ZIP8"Aged 80 and overGenetics0303 health sciences"mental brain homeostasis"; "psychosis"; "metal ion transporters"; "ZIP8"; "whole-genome assosiation"; "SLC39A3"Zip8 protein humanMiddle Aged3. Good health"whole-genome assosiation"SpainCase-Control StudiesSchizophreniaFemale"SLC39A3""metal ion transporters"030217 neurology & neurosurgeryBiological Psychiatry
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Lack of efficacy of mitoxantrone in primary progressive Multiple Sclerosis irrespective of pharmacogenetic factors: A multi-center, retrospective ana…

2014

Abstract Background Mitoxantrone is used on an off-label basis in primary progressive MS (PPMS). ABC -transporter-genotypes are associated with therapeutic response in relapsing/secondary progressive MS (RP/SPMS). Objective To evaluate potential pharmacogenetic response markers for mitoxantrone in PPMS. Methods 41 mitoxantrone-treated PPMS-patients, 155 mitoxantrone-treated RP/SPMS-patients and 43 PPMS-controls were retrospectively assessed for clinical therapy-response and in correlation with four single-nucleotide-polymorphisms in ABCB1 - and ABCG2 -genes. Results 53.7% PPMS-patients were mitoxantrone-responders, in comparison to 78.1% of RP/SPMS-patients (p = 0.039). There was no associa…

AdultMaleOncologymedicine.medical_specialtyTreatment responseATP Binding Cassette Transporter Subfamily Bmedicine.medical_treatmentImmunologyPrimary Progressive Multiple SclerosisPharmacologyInternal medicineGenotypeLack of efficacymedicineRetrospective analysisATP Binding Cassette Transporter Subfamily G Member 2HumansImmunology and AllergyRetrospective StudiesAnalgesicsMitoxantronebusiness.industryImmunosuppressionMiddle AgedMultiple Sclerosis Chronic ProgressiveNeoplasm Proteins3. Good healthNeurologyPharmacogeneticsATP-Binding Cassette TransportersFemaleNeurology (clinical)MitoxantronebusinessPharmacogeneticsmedicine.drugJournal of Neuroimmunology
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Recessive multiple epiphyseal dysplasia (rMED): phenotype delineation in eighteen homozygotes for DTDST mutation R279W.

2003

Multiple epiphyseal dysplasia (MED) is a generalised skeletal dysplasia that although relatively mild is associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. In the past, the disorder was subdivided into the milder Ribbing type, usually with flattened epiphyses,1 and the more severe Fairbank type with round epiphyses,2 but many cases were not classifiable as clearly either type.3 MED can be caused by mutations in at least six separate genes: COMP ,4–7 collagen IX ( COL9A1 , COL9A2 , and COL9A3 ),8–13 matrilin 3 ( MATN3 ),15 and the sulphate transporter, DTDST ( DTDST/SLC26A2 ). We have previously repor…

AdultMalePathologymedicine.medical_specialtyAdolescentAnion Transport ProteinsGenes RecessiveBiologySLC26A2ArginineOsteochondrodysplasiasShort statureMultiple epiphyseal dysplasiaGeneticsmedicineHumansChildGenetics (clinical)GeneticsAchondrogenesisSulfatesPoint mutationHomozygoteTryptophanChromosome MappingMembrane Transport ProteinsBiological TransportMiddle Agedmedicine.diseasePhenotypeGenetic defects of metabolism [UMCN 5.1]Amino Acid SubstitutionDysplasiaSulfate TransportersMutation (genetic algorithm)MutationMutation testingbiology.proteinFemalemedicine.symptomCarrier ProteinsLetter to JMGJournal of medical genetics
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Defects in the Human Leukocyte Antigen Class I Antigen Processing Machinery in Head and Neck Squamous Cell Carcinoma: Association with Clinical Outco…

2005

AbstractPurpose: Human leukocyte antigen (HLA) class I antigen defects, which are frequently present in head and neck squamous cell carcinoma (HNSCC) cells may provide the tumor with an escape mechanism from immune surveillance. Scanty information is available about mechanisms underlying HLA class I antigen defects in both lesions and cell lines from HNSCC. In this study, we investigate the role of antigen processing machinery (APM) component abnormalities in the generation of deficient HLA class I surface expression of HNSCC cells.Experimental Design: Using immunohistochemistry, Western blot, and RT-PCR analyses we correlated the expression of the IFN-γ inducible proteasome subunits and of…

AdultMaleProteasome Endopeptidase ComplexCancer ResearchPathologymedicine.medical_specialtyBlotting WesternDown-RegulationHuman leukocyte antigenBiologyCell LineInterferon-gammaATP Binding Cassette Transporter Subfamily B Member 3HLA AntigensMultienzyme ComplexesCell Line TumorTumor Cells Culturedotorhinolaryngologic diseasesmedicineCarcinomaHumansATP Binding Cassette Transporter Subfamily B Member 2AgedReverse Transcriptase Polymerase Chain ReactionAntigen processingHistocompatibility Antigens Class ICancerMiddle Agedmedicine.diseaseImmunohistochemistrySurvival AnalysisHead and neck squamous-cell carcinomaGene Expression Regulation NeoplasticCysteine Endopeptidasesstomatognathic diseasesOncologyHead and Neck NeoplasmsCarcinoma Squamous Cellbiology.proteinImmunohistochemistryTAP2ATP-Binding Cassette TransportersFemaleTAP1Clinical Cancer Research
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High-dose short-term administration of naringin did not alter talinolol pharmacokinetics in humans.

2015

Naringin is considered the major causative ingredient of the inhibition of intestinal drug uptake by grapefruit juice. Moreover, it is contained in highly dosed nutraceuticals available on the market. A controlled, open, randomized, crossover study was performed in 10 healthy volunteers to investigate the effect of high-dose naringin on the bioavailability of talinolol, a substrate of intestinal organic anion-transporting polypeptide (OATP)-mediated uptake. Following 6-day supplementation with 3 capsules of 350 mg naringin daily, 100mg talinolol were administered orally with 3 capsules of the same dietary supplement (1050 mg naringin) on the seventh day. This test treatment was compared to …

AdultMalefood.ingredientAdrenergic beta-AntagonistsPharmaceutical ScienceOrganic Anion TransportersPharmacologyPolymorphism Single NucleotideDosage formGrapefruit juicePropanolamineschemistry.chemical_compoundFood-Drug InteractionsYoung AdultNutraceuticalfoodPharmacokineticsHumansNaringinDosage FormsCross-Over StudiesDose-Response Relationship DrugChemistryCrossover studyBioavailabilityDietary SupplementsFlavanonesFemaleTalinololCitrus paradisiEuropean journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
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Familial HDL deficiency due to ABCA1 gene mutations with or without other genetic lipoprotein disorders

2004

Mutations in ABCA1 have been shown to be the cause of Tangier disease (TD) and some forms of familial hypoalphalipoproteinemia (HA), two genetic disorders characterized by low plasma HDL levels. Here we report six subjects with low HDL, carrying seven ABCA1 mutations, six of which are previously unreported. Two mutations (R557X and H160FsX173) were predicted to generate short truncated proteins; two mutations (E284K and Y482C) were located in the first extracellular loop and two (R1901S and Q2196H) in the C-terminal cytoplasmic domain of ABCA1. Two subjects found to be compound heterozygotes for ABCA1 mutations did not have overt clinical manifestations of TD. Three subjects, all with prema…

AdultMalemedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BAdolescentPremature coronary artery diseaseTangier diseaseCoronary DiseaseBiologyGene mutationmedicine.disease_causeCompound heterozygosityTangier diseaseInternal medicineGenotypeABCA1 genemedicineHumansChildHypoalphalipoproteinemiaSelection BiasAgedApolipoproteins BGeneticsMutationFamilial defective Apo B (FDB)Apolipoprotein A-ICholesterol HDLnutritional and metabolic diseasesMiddle Agedmedicine.diseaseLipoprotein lipaseTangier disease; Familial HDL deficiency; ABCA1 gene; Familial defective Apo B (FDB); Lipoprotein lipase; Premature coronary artery diseaseEndocrinologyChild PreschoolMutationbiology.proteinlipids (amino acids peptides and proteins)Allelic heterogeneityATP-Binding Cassette TransportersFemaleCardiology and Cardiovascular MedicineFamilial HDL deficiencyATP Binding Cassette Transporter 1
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Association of selected ABC gene family single nucleotide polymorphisms with postprandial lipoproteins: results from the population-based Hortega stu…

2009

The aim of the study was to determine the influence of twenty single nucleotide polymorphisms (SNPs) of the ABCA1, ABCG1, ABCG5 and ABCG8 genes on the plasmatic concentrations of total cholesterol (TC), HDL and LDL cholesterol (HDLc, LDLc) in the postprandial state with a representative Spanish Caucasian population (1473 individuals, 50.0% women, ages ranging 21-85 years). In men, subjects with the AA genotype of the ABCA1 rs2230806 (R219K) polymorphism were associated with increased plasma LDLc levels, while the ABCA1 haplotype, which included the rs2230806 A allele, was associated with higher TC and LDLc plasma concentrations. In women, significant relationships were found between rs18935…

AdultMalemedicine.medical_specialtyLipoproteinsBlood lipidsSingle-nucleotide polymorphismHyperlipidemiasBiologyPolymorphism Single Nucleotidechemistry.chemical_compoundHigh-density lipoproteinPolymorphism (computer science)Internal medicineGenotypemedicineHumansATP Binding Cassette Transporter Subfamily G Member 5AllelesATP Binding Cassette Transporter Subfamily G Member 1AgedGeneticsAged 80 and overCholesterolHaplotypeATP Binding Cassette Transporter Subfamily G Member 8Cholesterol HDLMiddle AgedAtherosclerosisPostprandial PeriodPostprandialEndocrinologyCholesterolchemistryHaplotypesSpainlipids (amino acids peptides and proteins)ATP-Binding Cassette TransportersFemaleCardiology and Cardiovascular MedicineATP Binding Cassette Transporter 1Atherosclerosis
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Intrafamilial variability of the deafness and goiter phenotype in Pendred syndrome caused by a T416P mutation in the SLC26A4 gene.

2004

AbstractPendred syndrome (PS) is the most common cause of syndromic deafness, accounting for more than 5% of all autosomal-recessive hearing loss cases. It is characterized by bilateral sensorineural hearing loss and by goiter with or without hypothyroidism. Mutations in the SLC26A4 gene cause both classical PS and deafness associated with an enlarged vestibular aqueduct without goiter.To investigate a possible genotype-phenotype correlation in PS, we performed a detailed clinical and genetic study in three adult German sibs with typical PS caused by a common homozygous SLC26A4 mutation, T416P. An audiological long-term follow-up of 23 yr showed that the mutation T416P is associated with a …

AdultMalemedicine.medical_specialtyVestibular aqueductGoiterAdolescentHearing lossEndocrinology Diabetes and Metabolismmedicine.medical_treatmentHearing Loss SensorineuralClinical BiochemistryThyroid GlandDeafnessBiochemistryConnexinsEndocrinologyInternal medicineotorhinolaryngologic diseasesmedicineHumansChildPendred syndromebusiness.industryGoiterBiochemistry (medical)ThyroidThyroidectomyMembrane Transport ProteinsSyndromemedicine.diseaseConnexin 26Endocrinologymedicine.anatomical_structurePhenotypeSulfate TransportersChild PreschoolMutationSensorineural hearing lossFemalemedicine.symptombusinessEnlarged vestibular aqueductThe Journal of clinical endocrinology and metabolism
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