Search results for "binding proteins"

showing 10 items of 911 documents

Bcl-6 mutation status provides clinically valuable information in early-stage B-cell chronic lymphocytic leukemia

2004

In B-cell chronic lymphocytic leukemia (B-CLL), somatic mutation of IgVH genes defines a subgroup with favorable prognosis, whereas the absence of IgVH mutations is correlated with a worse outcome. Mutations of the BCL-6 gene are also observed in a subset of B-CLL, but the clinical significance of this molecular alteration remains uncertain. We examined the distribution of IgVH and BCL-6 gene mutations in 95 well-characterized patients with Binet stage A B-CLL, and correlated them with clinical, laboratory, cytogenetic findings and disease progression. Mutations of the BCL-6 gene were observed only in cases harboring mutated IgVH. Unexpectedly, coexistence of IgVH and BCL-6 mutations was co…

AdultMaleOncologyCancer Researchmedicine.medical_specialtyChronic lymphocytic leukemiaImmunoglobulin Variable RegionLocus (genetics)BiologyGene mutationDisease-Free SurvivalGermline mutationProto-Oncogene ProteinsInternal medicinemedicineHumansB-cell chronic lymphocytic leukemiaClinical significanceProspective StudiesGeneAgedAged 80 and overHematologyChromosomes Human Pair 11HematologyMiddle AgedPrognosismedicine.diseaseLeukemia Lymphocytic Chronic B-CellDNA-Binding ProteinsOncologyMutationImmunologyProto-Oncogene Proteins c-bcl-6FemaleChromosome DeletionChromosomes Human Pair 17Follow-Up StudiesTranscription FactorsLeukemia
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Molecular characterisation and expression analysis of SEREX-defined antigen NUCB2 in gastric epithelium, gastritis and gastric cancer.

2009

NUCB2 is an EF-hand Ca2+ binding protein that has been implicated in various physiological processes like calcium homeostasis, hypothalamic regulation of feeding and TNF receptor shedding. In our previous study we identified NUCB2 as a potential tumour antigen eliciting autoantibody responses in 5.4% of gastric cancer patients but not in the healthy individuals.The current study aimed to elucidate the molecular mechanism underlying NUCB2 immunogenicity and to gain an insight into the physiological functions of NUCB2 in the stomach. mRNA expression analysis demonstrated that NUCB2 is ubiquitously expressed in normal tissues, including lymphoid tissues, and downregulated in gastric tumours wh…

AdultMalePathologymedicine.medical_specialtyHistologyNUCB2BiophysicsDown-RegulationNerve Tissue ProteinsBiologyAntigenWestern blotchief cellsParietal Cells GastricStomach NeoplasmsGastric glandsGastric mucosamedicineHumansNucleobindinsEnterochromaffin-like celllcsh:QH301-705.5AgedAutoantibodiesAged 80 and overOriginal Papermedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionStomachgastric cancerCalcium-Binding Proteinsparietal cellsCell BiologySEREXMiddle AgedMolecular biologyGastric chief cellDNA-Binding Proteinsmedicine.anatomical_structurelcsh:Biology (General)Gastric MucosaGastritisCancer cellpepsinogen secretion.Femaletumour-associated antigensProtein Processing Post-TranslationalEuropean journal of histochemistry : EJH
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Variable phenotypic expression of chylomicron retention disease in a kindred carrying a mutation of the Sara2 gene

2010

Chylomicron retention disease is a recessive inherited disorder characterized by fat malabsorption and steatorrhea and is associated with failure to thrive in infancy. We describe a kindred carrying a mutation of Sara2 gene causing a chylomicron retention phenotype. The proband was a 5-month-old baby, born of consanguineous, apparently healthy parents from Morocco, with failure to thrive. There was a large quantity of fats in feces and malabsorption of fat-soluble vitamins. Intestinal biopsies showed a diffused enterocyte vacuolization with large cytosolic lipid droplets. Chylomicron retention disease or Anderson disease was hypothesized, and the Sara2 gene was analyzed by direct sequencing…

AdultMaleProbandmedicine.medical_specialtychylomicron retention disease phenotypic expression Sara2Settore MED/09 - Medicina InternaMalabsorptionEndocrinology Diabetes and MetabolismBiologySettore MED/42 - Igiene Generale E ApplicataExonEndocrinologyMalabsorption SyndromesInternal medicineChylomicronsmedicineHumansAlleleMonomeric GTP-Binding ProteinsGeneticsHaplotypeInfantmedicine.diseaseSteatorrheaPedigreeFat malabsorptionPhenotypeEndocrinologyChild PreschoolMutationFailure to thriveFabry DiseaseFemalemedicine.symptomChylomicron retention diseaseMetabolism
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Mutations in ARL2BP, Encoding ADP-Ribosylation-Factor-Like 2 Binding Protein, Cause Autosomal-Recessive Retinitis Pigmentosa

2013

Retinitis pigmentosa (RP) is a genetically heterogeneous retinal degeneration characterized by photoreceptor death, which results in visual failure. Here, we used a combination of homozygosity mapping and exome sequencing to identify mutations in ARL2BP, which encodes an effector protein of the small GTPases ARL2 and ARL3, as causative for autosomal-recessive RP (RP66). In a family affected by RP and situs inversus, a homozygous, splice-acceptor mutation, c.101−1G>C, which alters pre-mRNA splicing of ARLBP2 in blood RNA, was identified. In another family, a homozygous c.134T>G (p.Met45Arg) mutation was identified. In the mouse retina, ARL2BP localized to the basal body and cilium-associated…

AdultMaleRetinal degenerationCentrioleMolecular Sequence DataGenes RecessiveBiologymedicine.disease_causeMice03 medical and health sciences0302 clinical medicineBardet–Biedl syndromeGTP-Binding ProteinsReportRetinitis pigmentosaGeneticsmedicineAnimalsHumansBasal bodyGenetics(clinical)Photoreceptor CellsGenetics (clinical)030304 developmental biologyPrimary ciliary dyskinesiaGenetics0303 health sciencesMutationBase SequenceADP-Ribosylation FactorsCiliumHomozygoteMembrane Transport ProteinsEpithelial Cellsmedicine.diseasePedigreeCell biologyMutationFemalesense organsCarrier ProteinsRetinitis Pigmentosa030217 neurology & neurosurgeryProtein BindingTranscription FactorsThe American Journal of Human Genetics
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Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation: Evidence in Crohn diseas…

2000

The pro-inflammatory cytokine interleukin (IL)-6 (refs. 1-5) can bind to cells lacking the IL-6 receptor (IL-6R) when it forms a complex with the soluble IL-6R (sIL-6R) (trans signaling). Here, we have assessed the contribution of this system to the increased resistance of mucosal T cells against apoptosis in Crohn disease (CD), a chronic inflammatory disease of the gastrointestinal tract. A neutralizing antibody against IL-6R suppressed established experimental colitis in various animal models of CD mediated by type 1 T-helper cells, by inducing apoptosis of lamina propria T cells. Similarly, specific neutralization of sIL-6R in vivo by a newly designed gp130-Fc fusion protein caused suppr…

AdultMaleSTAT3 Transcription FactorT-Lymphocytesmedicine.medical_treatmentT cellbcl-X ProteinApoptosisGeneral Biochemistry Genetics and Molecular BiologyMiceCrohn DiseaseAntigenAntigens CDCytokine Receptor gp130medicineAnimalsHumansInterleukin 6Mice Inbred BALB CMembrane GlycoproteinsbiologyInterleukin-6Models ImmunologicalInterleukinGeneral MedicineMiddle AgedReceptors Interleukin-6DNA-Binding ProteinsCytokinemedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisImmunologyTrans-Activatorsbiology.proteinSTAT proteinCancer researchColitis UlcerativeFemaleSignal transductionProtein BindingSignal TransductionNature Medicine
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Influence of sex and genetic variability on expression of X-linked genes in human monocytes

2011

Abstract In humans, the fraction of X-linked genes with higher expression in females has been estimated to be 5% from microarray studies, a proportion lower than the 25% of genes thought to escape X inactivation. We analyzed 715 X-linked transcripts in circulating monocytes from 1,467 subjects and found an excess of female-biased transcripts on the X compared to autosomes (9.4% vs 5.5%, p  −5 ). Among the genes not previously known to escape inactivation, the most significant one was EFHC2 whose 20% of variability was explained by sex. We also investigated cis expression quantitative trait loci (eQTLs) by analyzing 15,703 X-linked SNPs. The frequency and magnitude of X-linked cis eQTLs were…

AdultMaleTranscription GeneticMicroarrayQuantitative Trait LociSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideMonocytesX-inactivationSex FactorsGenes X-LinkedX Chromosome InactivationGene expressionGeneticsHumansGenetic variabilityGeneAgedGeneticsChromosomes Human XAutosomeCalcium-Binding ProteinsGenderGenetic VariationMiddle AgedExpression Quantitative Trait LocusExpression quantitative trait lociFemaleGene expressionGenome-Wide Association StudyGenomics
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Retinol oxidation to retinoic acid in human thyroid glandular cells.

2014

Abstract Retinoic acid is regarded as the retinol metabolite that controls proliferation and differentiation of epithelial cells. In the present study, we investigated the potential role of xanthine dehydrogenase (XDH) in retinoic acid biosynthesis in human thyroid glandular cells (HTGC). In particular, we observed that cellular retinoids binding proteins (CRBPs) are also implicated in the biosynthetic pathway leading to retinoic acid formation in primary cultures of HTGC, as we have already reported for human mammary epithelial cells (HMEC). After partial protein purification, the enzyme responsible for retinoic acid biosynthesis was identified and quantified as XDH by immunoassay, by its …

AdultMaleXanthine DehydrogenasePrimary Cell CultureRetinoic acidThyroid GlandOxypurinolRetinoic acid receptor betaTretinoinBiologyXanthinechemistry.chemical_compoundBiosynthesisSettore BIO/10 - BiochimicaDrug DiscoveryHumansEnzyme InhibitorsVitamin AEnzyme AssaysPharmacologyImmunoassayRetinolEpithelial CellsRetinol-Binding Proteins CellularGeneral MedicineMiddle AgedXanthineUric AcidRetinoic acid receptorchemistryXanthine dehydrogenaseBiochemistryCRABPs CRBPs human glandular cells. retinoic acid biosynthesis. retinol oxidation xanthine dehydrogenaseUric acidFemaleOxidation-ReductionJournal of enzyme inhibition and medicinal chemistry
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Genotypic and phenotypic spectrum in tricho-rhino-phalangeal syndrome types I and III

2000

Tricho-rhino-phalangeal syndrome (TRPS) is characterized by craniofacial and skeletal abnormalities. Three subtypes have been described: TRPS I, caused by mutations in the TRPS1 gene on chromosome 8; TRPS II, a microdeletion syndrome affecting the TRPS1 and EXT1 genes; and TRPS III, a form with severe brachydactyly, due to short metacarpals, and severe short stature, but without exostoses. To investigate whether TRPS III is caused by TRPS1 mutations and to establish a genotype-phenotype correlation in TRPS, we performed extensive mutation analysis and evaluated the height and degree of brachydactyly in patients with TRPS I or TRPS III. We found 35 different mutations in 44 of 51 unrelated p…

AdultMaleanimal structuresAdolescentGenotypeDNA Mutational AnalysisMolecular Sequence DataLimb Deformities CongenitalBiologyOsteochondrodysplasiasPolymorphism Single NucleotideShort statureLanger–Giedion syndromeGeneticsmedicineHumansMissense mutationTricho–rhino–phalangeal syndromeGenetics(clinical)Amino Acid SequenceChildGenetics (clinical)GeneticsAnthropometryBase SequenceBrachydactylyInfantZinc FingersExonsSyndromeArticlesMiddle AgedMicrodeletion syndromemedicine.diseasePenetranceBody HeightPedigreeDNA-Binding ProteinsRadiographyPhenotypeChild PreschoolMutationTrichorhinophalangeal Syndrome Type IErythroid-Specific DNA-Binding FactorsFemalemedicine.symptomChromosomes Human Pair 8Transcription Factors
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Congenital goitrous primary hypothyroidism in two German families caused by novel thyroid peroxidase (TPO) gene mutations.

2013

Congenital hypothyroidism occurs with a prevalence of approximately 1:3 500. Defects in thyroid hormone synthesis which lead to goitrous hypothyroidism account for 10-15% of these cases. Several genetic defects have been characterized and mutations in the thyroid peroxidase (TPO) gene are the most common cause for dyshormonogenesis.So far, more than 80 mutations in the TPO gene have been described, resulting in a variable decrease in TPO bioactivity. Clinically TPO defects manifest with congenital primary goitrous hypothyroidism.We here present 2 children with congenital primary hypothyroidism, who were identified to have compound heterozygous TPO mutations. They both shared the same novel …

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismMutation MissenseGene mutationmedicine.disease_causeCompound heterozygosityAutoantigensIodide Peroxidasefluids and secretionsEndocrinologyThyroid dyshormonogenesisThyroid peroxidaseInternal medicineGermanyIron-Binding ProteinsInternal MedicinemedicineCongenital HypothyroidismMissense mutationHumansFamilyMutationbiologybusiness.industryGoiterPrimary hypothyroidismInfant Newbornfood and beveragesGeneral MedicineExonsmedicine.diseaseCongenital hypothyroidismEndocrinologyembryonic structuresbiology.proteinFemalebusinessExperimental and clinical endocrinologydiabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
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Ten novel mutations found in Aniridia.

1998

Aniridia (AN) is a sight-threatening congenital ocular disorder characterized by iris hypoplasia, corneal pannus, foveal and optic nerve hypoplasia, cataract formation, and glaucoma. In two-thirds of the patients, AN is inherited in an autosomal dominant fashion with almost complete penetrance but variable expression. The remaining cases are sporadic. Aniridia has been shown to be associated with mutations in the PAX6 gene, located on chromosome 11p13, telomeric to the Wilms' tumor predisposition gene (WT1). This paper describes 14 mutations in the PAX6 gene in patients with AN. Among these 14 mutations, 10 have been unpublished until now. They result most probably in haploinsufficiency and…

AdultMalegenetic structuresAdolescentPAX6 Transcription FactorDNA Mutational AnalysisMolecular Sequence DataBiologyPolymerase Chain ReactionVariable ExpressionGeneticsmedicineHumansPaired Box Transcription FactorsAmino Acid SequenceChildEye ProteinsGeneAniridiaGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsHomeodomain ProteinsOptic nerve hypoplasiaInfantMiddle Agedmedicine.diseasePenetranceeye diseasesDNA-Binding ProteinsRepressor ProteinsAniridiaChild PreschoolMutationHomeoboxFemalesense organsPAX6HaploinsufficiencyTranscription FactorsHuman mutation
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