Search results for "splice"

showing 10 items of 53 documents

Voltage dependence of L-arginine transport by hCAT-2A and hCAT-2B expressed in oocytes from Xenopus laevis.

2000

Membrane potential and currents were investigated with the two-electrode voltage-clamp technique in Xenopus laevisoocytes expressing hCAT-2A or hCAT-2B, the splice variants of the human cationic amino acid transporter hCAT-2. Both hCAT-2A- and hCAT-2B-expressing oocytes exhibited a negative extracellularl-arginine concentration ([l-Arg]o)-sensitive membrane potential, additive to the K+diffusion potential, when cells were incubated in Leibovitz medium (containing 1.45 mM l-Arg and 0.25 mM l-lysine). The two carrier proteins produced inward and outward currents, which were dependent on the l-Arg gradient and membrane potential. Ion substitution experiments showed that the hCAT-induced curren…

ArgininePhysiologyXenopusBiologyArginineL-arginine transportXenopus laevisElectrochemistryAnimalsHumansProtein IsoformsspliceAmino acid transporterMembrane potentialMembrane ProteinsBiological TransportCell BiologyMembrane transportbiology.organism_classificationIn vitroCell biologyElectrophysiologyKineticsBiochemistryOocytesAmino Acid Transport Systems BasicFemaleCarrier ProteinsAmerican journal of physiology. Cell physiology
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Characterisation of tumour-associated antigens in colon cancer.

2002

In order to search for clinically relevant cancer-associated genes and to define further the spectrum of immunogenic proteins, we applied SEREX (serological identification of antigens by recombinant expression cloning) to analyse genes expressed in colon adenocarcinoma. Eight different serum-reactive cDNA clones were isolated by immunoscreening from a colon cancer-derived cDNA expression library. mRNA expression studies showed that 2 of them, RHAMM and AD034, have a differential tissue distribution, and that 3 genes, NAP1L1, RHAMM and AD034, are overexpressed in tumours in comparison with the adjacent non-cancerous tissues. 5' RLM-RACE analysis of AD034, a sequence with a tyrosine kinase mo…

Cancer ResearchAntibodies NeoplasmImmunologyMolecular Sequence DataBiologyAdenocarcinomaProtein Serine-Threonine KinasesAntigenAntigens NeoplasmIsoantibodiesComplementary DNAImmunoscreeningGene expressionmedicineImmunology and AllergyHumansspliceTissue DistributionRNA MessengerCloning MolecularGeneGene LibraryGeneticsExtracellular Matrix ProteinsCancermedicine.diseaseMolecular biologyAlternative SplicingHyaluronan ReceptorsOncologyColonic NeoplasmsAdenocarcinomaCancer immunology, immunotherapy : CII
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Expression of IAPs and alternative splice variants in hepatocellular carcinoma tissues and cells.

2005

IAPs (inhibitors of apoptosis proteins) might have a major role in the apoptotic resistance that marks many cancers. The studies on IAPs in human HCC have focused on survivin or XIAP, indicating that their new or increased expression in this tumor is associated with a more unfavorable prognosis. The present results corroborate these findings, emphasizing the role that the coordinated expression of different IAPs and alternative splice variants might play in the adverse biology of hepatocellular carcinoma.

Carcinoma HepatocellularApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyBioinformaticsGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceCell Line TumorSurvivinCarcinomamedicineHumansspliceRNA MessengerCell ProliferationCell growthReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceAlternative splicingLiver NeoplasmsIntracellular Signaling Peptides and ProteinsProteinsmedicine.diseasePrognosisXIAPbody regionsAlternative SplicingApoptosisDrug Resistance NeoplasmHepatocellular carcinomaCancer researchAnnals of the New York Academy of Sciences
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Novel form of X-linked nonsyndromic hearing loss with cochlear malformation caused by a mutation in the type IV collagen gene COL4A6

2013

Hereditary hearing loss is the most common human sensorineural disorder. Genetic causes are highly heterogeneous, with mutations detected in >40 genes associated with nonsyndromic hearing loss, to date. Whereas autosomal recessive and autosomal dominant inheritance is prevalent, X-linked forms of nonsyndromic hearing impairment are extremely rare. Here, we present a Hungarian three-generation family with X-linked nonsyndromic congenital hearing loss and the underlying genetic defect. Next-generation sequencing and subsequent segregation analysis detected a missense mutation (c.1771G>A, p.Gly591Ser) in the type IV collagen gene COL4A6 in all affected family members. Bioinformatic analysis an…

Collagen Type IVMaleHearing lossDNA Mutational AnalysisMolecular Sequence DataMutation MissenseGene ExpressionDeafnessBiologyCongenital hearing lossmedicine.disease_causeArticleType IV collagenotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMissense mutationGenetic Predisposition to DiseaseAmino Acid SequenceAlport syndromeGeneCells CulturedGenetic Association StudiesZebrafishGenetics (clinical)GeneticsMutationGenetic Diseases X-LinkedMiddle Agedmedicine.diseaseCochleaPedigreeMice Inbred C57BLChild PreschoolFemaleRNA Splice SitesOtic vesiclemedicine.symptomEuropean Journal of Human Genetics
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Expression analysis and functional activity of interleukin-7 splice variants.

2008

Alternative splicing results in multiple protein isoforms derived from a single gene. The magnitude of this process ranges from a complete loss of function to gain of new function. We examined, as a paradigm, alternative splicing of the non-redundant human cytokine, interleukin-7 (IL-7). We show that extensive IL-7 splicing in human tissues of different histology, including MTB+ granuloma lesions, transformed tissue and tumor cell lines. IL-7 splice variants were expressed as recombinant proteins. A differentially spliced IL-7 isoform, lacking exon 5, leads to STAT-5 phosphorylation in CD4+ and CD8+ T cells, promotes thymocyte maturation and T-cell survival. Human tumor lesions show aberran…

Gene isoformCD4-Positive T-LymphocytesCell SurvivalImmunologyBiologyCD8-Positive T-LymphocytesExonCell Line TumorGeneticsSTAT5 Transcription FactorHumansProtein IsoformssplicePhosphorylationGenetics (clinical)GranulomaInterleukin-7Alternative splicingInterleukinExonsMolecular biologyRecombinant ProteinsCell biologyThymocyteAlternative SplicingOrgan SpecificityRNA splicingCD8Genes and immunity
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Evaluating the effect of spastin splice mutations by quantitative allele-specific expression assay

2010

Background:  Mutations in the SPG4/SPAST gene are the most common cause for hereditary spastic paraplegia (HSP). The splice-site mutations make a significant contribution to HSP and account for 17.4% of all types of mutations and 30.8% of point mutations in the SPAST gene. However, only few studies with limited molecular approach were conducted to investigate and decipher the role of SPAST splice-site mutations in HSP. Methods:  A reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and quantitative allele-specific expression assay were performed. Results:  We have characterized the consequence of two novel splice-site mutations (c.1493 + 1G>A and c.1414−1G>A) in the SPAST gene…

Genetics0303 health sciencesbusiness.industryHereditary spastic paraplegiaPoint mutationSpastinmedicine.disease03 medical and health sciencesExon0302 clinical medicineNeurologyRNA splicingMedicinespliceNeurology (clinical)businessSPAST gene030217 neurology & neurosurgeryAllele specific030304 developmental biologyEuropean Journal of Neurology
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Alterations of pre-mRNA splicing in cancer

2005

Recent genomewide analyses of alternative splicing (AS) indicate that up to 70% of human genes may have alternative splice forms, suggesting that AS together with various posttranslational modifications plays a major role in the production of proteome complexity. Splice-site selection under normal physiological conditions is regulated in the developmental stage in a tissue type-specific manner by changing the concentrations and the activity of splicing regulatory proteins. Whereas spliceosomal errors resulting in the production of aberrant transcripts rarely occur in normal cells, they seem to be an intrinsic property of cancer cells. Changes in splice-site selection have been observed in v…

GeneticsCancer ResearchRNA SplicingAlternative splicingExonic splicing enhancerIntronExonsBiologymedicine.disease_causeIntronsCell biologyExonTumor progressionRNA splicingRNA PrecursorsGeneticsmedicineHumansspliceCarcinogenesisGenes, Chromosomes and Cancer
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Intronic L1 insertion and F268S, novel mutations in RPS6KA3 (RSK2) causing Coffin-Lowry syndrome

2003

Two novel mutations of the ribosomal S6 kinase 2 gene (also known as RSK2) have been identified in two unrelated patients with Coffin–Lowry syndrome. The first mutation consists of a de novo insertion of a 5′-truncated LINE-1 element at position −8 of intron 3, which leads to a skipping of exon 4, leading to a shift of the reading frame and a premature stop codon. The L1 fragment (2800 bp) showed a rearrangement with a small deletion, a partial inversion of the ORF 2, flanked by short direct repeats which duplicate the acceptor splice site. However, cDNA analysis of the patient shows that both sites are apparently not functional. The second family showed the nucleotide change 803T>C in exon…

GeneticsCoffin–Lowry syndromeMutationSplice site mutationIntronMonozygotic twinBiologymedicine.diseasemedicine.disease_causeExonRPS6KA3GeneticsmedicineDirect repeatGenetics (clinical)Clinical Genetics
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The human complement C9 gene: structural analysis of the 5′ gene region and genetic polymorphism studies

2001

Summary C9 is the last of the human complement components creating the membrane attack complex. The single chain serum protein is encoded by a gene located on chromosome 5p13 that is composed of 11 exons. With the aid of inverse PCR, the hitherto unknown regions flanking exon 1 and the 3′ part of exon 11 (3′UTR) have been sequenced. A computer-based analysis of the 300-bp region located just upstream of the AUG start codon showed homologies to known DNA modules which affect the transcriptional regulation of certain genes. The most striking of these is a sequence that may substitute the missing TATA box in initiating C9 transcription. In the 3′UTR, three successive polyadenylation signals we…

GeneticsExonExon trappingSplice site mutationImmunologyGeneticsIntronSingle-nucleotide polymorphismTandem exon duplicationBiologyExon shufflingGeneMolecular biologyEuropean Journal of Immunogenetics
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Five Novel Mutations in F13B Gene Resulting in Mild FXIII Deficiency

2008

FXIII deficiency is a rare autosomal recessive disorder affecting approximately 1 out of 1–3 million inhabitants. The disease is characterized by bleeding, impaired wound repair and spontaneous abortions in females. Extracellular FXIII molecule has a tetramer structure composing of two catalytic A-subunits and two B-subunits that act as a carrier molecule. Based on genotype there are two types of FXIII deficiency: A-subunit deficiency (XIIIA) when mutations affect F13A gene and much rarely B-subunit deficiency (XIIIB) when mutations affect F13B gene. Both types result in absence of FXIII catalytical activity in plasma.

GeneticsSplice site mutationGenotypeIntronExtracellularMissense mutationHeterozygote advantageBiologyGene
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