Search results for " transporters"

showing 10 items of 194 documents

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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C4-dicarboxylate carriers and sensors in bacteria

2002

AbstractBacteria contain secondary carriers for the uptake, exchange or efflux of C4-dicarboxylates. In aerobic bacteria, dicarboxylate transport (Dct)A carriers catalyze uptake of C4-dicarboxylates in a H+- or Na+-C4-dicarboxylate symport. Carriers of the dicarboxylate uptake (Dcu)AB family are used for electroneutral fumarate:succinate antiport which is required in anaerobic fumarate respiration. The DcuC carriers apparently function in succinate efflux during fermentation. The tripartite ATP-independent periplasmic (TRAP) transporter carriers are secondary uptake carriers requiring a periplasmic solute binding protein. For heterologous exchange of C4-dicarboxylates with other carboxylic …

Aerobic bacteriaAntiporterSuccinic AcidBiophysicsOrganic Anion TransportersReceptors Cell Surfacemedicine.disease_causeBiochemistryFumarate (succinate) sensorTwo-component systemBacterial ProteinsFumaratesEscherichia colimedicineAmino Acid SequenceEscherichia coliDicarboxylate uptake SHistidine protein kinasePhylogenyHistidineDicarboxylic Acid TransportersDicarboxylate transport BbiologyEscherichia coli ProteinsBiological TransportPeriplasmic spaceCell Biologybiology.organism_classificationTwo-component regulatory systemBacteria AerobicModels ChemicalBiochemistryAntiportFumarate/succinate transportEffluxDicarboxylate uptake carrierProtein KinasesDicarboxylate transport A carrierBacteriaSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Anxiolytic-like effects of acute and chronic GABA transporter inhibition in rats.

2002

Acute GABA transporter inhibition can induce anxiolytic-like behaviors. The present analysis addressed whether chronic treatment (23 days via drinking water) with a GABA transporter inhibitor affects rat behavior similar to acute treatment and interferes with additional benzodiazepine-receptor agonistic treatment. Seventy-one rats divided into seven groups were acutely treated with either vehicle, diazepam (2 mg/kg), zolpidem (0.05 mg/kg), tiagabine (19 mg/kg) or chronically with tiagabine with or without acute diazepam or zolpidem. Animals were behaviorally characterized in an elevated plus-maze. None of the treatments induced changes in the activity of the animals. Acute and chronic treat…

AgonistMalemedicine.medical_specialtyElevated plus mazeZolpidemGABA Plasma Membrane Transport ProteinsTime FactorsTiagabinemedicine.drug_classPyridinesNipecotic AcidsOrganic Anion TransportersPharmacologyAnxiolyticDrug Administration Schedulechemistry.chemical_compoundInternal medicinemedicineGABA transporterAnimalsNeurotransmitterMaze LearningTiagabineBiological PsychiatryDiazepambiologyBehavior Animalbusiness.industryMembrane ProteinsMembrane Transport ProteinsDrug SynergismRats Inbred StrainsRatsZolpidemPsychiatry and Mental healthEndocrinologyNeurologychemistryAnti-Anxiety Agentsbiology.proteinNeurology (clinical)businessCarrier ProteinsDiazepammedicine.drugJournal of neural transmission (Vienna, Austria : 1996)
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LXR antagonists induce ABCD2 expression

2014

X-linked adrenoleukodystrophy (X-ALD) is a rare neurodegenerative disorder characterized by the accumulation of very-long-chain fatty acids resulting from a beta-oxidation defect. Oxidative stress and inflammation are also key components of the pathogenesis. X-ALD is caused by mutations in the ABCDI gene, which encodes for a peroxisomal half ABC transporter predicted to participate in the entry of VLCFA-CoA into the peroxisome, the unique site of their beta-oxidation. Two homologous peroxisomal ABC transporters, ABCD2 and ABCD3 have been proven to compensate for ABCD1 deficiency when overexpressed. Pharmacological induction of these target genes could therefore represent an alternative ther…

Agonistx-ald;very-long-chain fatty acid;lxr;hydroxycholesterol;abcd2medicine.medical_specialtymedicine.drug_classx-aldEndogenyContext (language use)ATP-binding cassette transporterBiologyATP Binding Cassette Transporter Subfamily DInternal medicinemedicineHumanslxr[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyhydroxycholesterolLiver X receptorAdrenoleukodystrophyMolecular Biology[SDV.BDD]Life Sciences [q-bio]/Development BiologyLiver X ReceptorsFatty AcidsBiologie du développementNeurosciencesCell BiologyHep G2 CellsPeroxisomemedicine.diseaseOrphan Nuclear ReceptorsDevelopment BiologyHydroxycholesterolsvery-long-chain fatty acidOxidative StressEndocrinologyGene Expression RegulationCell cultureabcd2Neurons and Cognition[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Cancer researchlipids (amino acids peptides and proteins)AdrenoleukodystrophyATP-Binding Cassette Transporters[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
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