Search results for "script"

showing 10 items of 5143 documents

PGC1α Regulates the Endothelial Response to Fluid Shear Stress via Telomerase Reverse Transcriptase Control of Heme Oxygenase-1

2021

AbstractFluid shear stress (FSS) is known to mediate multiple phenotypic changes in the endothelium. Laminar FSS (undisturbed flow) is known to promote endothelial alignment to flow that is key to stabilizing the endothelium and rendering it resistant to atherosclerosis and thrombosis. The molecular pathways responsible for endothelial responses to FSS are only partially understood. Here we have identified peroxisome proliferator gamma coactivator-1α (PGC-1α) as a flow-responsive gene required for endothelial flow alignment in vitro and in vivo. Compared to oscillatory FSS (disturbed flow) or static conditions, laminar FSS (undisturbed flow) increased PGC-1α expression and its transcription…

Heme oxygenasechemistry.chemical_compoundmedicine.anatomical_structureHMOX1EndotheliumKLF4In vivoChemistrymedicineLaminar flowTelomerase reverse transcriptaseHemeCell biology
researchProduct

The hematopoietic niche: a Drosophila model, at last.

2007

The niche provides a specialised microenvironment necessary for maintenance of stem cells in a non differentiated state. While the hematopoietic stem cell (HSC) niche in vertebrates was the first to be recognized, Drosophila niches supporting germline stem cells were characterised first. Recent evidence for the existence of a niche maintaining hematopoietic precursors in Drosophila opens the way to study in vivo the niche/hematopoietic precursors interactions. The availability of a large collection of cell markers, mutants and sophisticated genetic tools makes Drosophila an attractive model for investigating the cellular and molecular mechanisms that are involved in these interactions.

HemocytesCalcium-Binding ProteinsMembrane ProteinsHematopoietic Stem CellsLarvaModels Animal[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsDrosophila ProteinsIntercellular Signaling Peptides and Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyDrosophilaSerrate-Jagged Proteins[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBiomarkersJagged-1 ProteinTranscription FactorsCell cycle (Georgetown, Tex.)
researchProduct

Overexpression of STAT-1 by adenoviral gene transfer does not inhibit hepatitis B virus replication.

2006

Objectives Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral acitivity against HBV in vitro. Methods To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus ex…

Hepatitis B virusCarcinoma HepatocellularBlotting WesternGenetic Vectorsmedicine.disease_causeTransfectionVirus ReplicationVirusHepatitis B virus PRE betaAdenoviridaeOrthohepadnavirusInterferonmedicineTumor Cells CulturedAnimalsHumansCells CulturedHepatitis B virusHepatologybiologyLiver NeoplasmsGastroenterologyvirus diseasesHepatitis Bmedicine.diseasebiology.organism_classificationVirologyMolecular biologydigestive system diseasesIn vitroDucksSTAT1 Transcription FactorHepadnaviridaeGene Expression RegulationDNA ViralHepatocytesmedicine.drugEuropean journal of gastroenterologyhepatology
researchProduct

Molecular Epidemiology and Immunology of Hepatitis B Virus Infection – An Update

2003

Hepatitis B virus (HBV) continues to be one of the most important viral pathogens in humans. This review provides an update on the molecular epidemiology and immunology of HBV infection. DNA sequencing has allowed replacement of the initial serotypic classification of HBV strains by a more systematic genotype system that currently consists of 7 members (genotypes A–G). More recently, sequence analysis of virus isolates from many individual patients has revealed the occurrence of certain mutational hot spots in the genome, some of which appear to correlate with the patient’s immunological and/or disease status; however, cause and effect are not always easily discernible. This holds particula…

Hepatitis B virusGenotypeMolecular Sequence DataPopulationBiologymedicine.disease_causeVirusVirologyGenotypemedicineHumansAmino Acid SequencePromoter Regions GeneticeducationHepatitis B viruseducation.field_of_studyMutationMolecular epidemiologyViral Core ProteinsVirionHepatitis BVirologyReverse transcriptaseVaccinationInfectious DiseasesMutationImmunologyIntervirology
researchProduct

Hepatitis B subviral envelope particles use the COPII machinery for intracellular transport via selective exploitation of Sec24A and Sec23B

2020

Hepatitis B virus (HBV) is a leading cause of liver disease. Its success as a human pathogen is related to the immense production of subviral envelope particles (SVPs) contributing to viral persistence by interfering with immune functions. To explore cellular pathways involved in SVP formation and egress, we investigated host-pathogen interactions. Yeast-based proteomics revealed Sec24A, a component of the coat protein complex II (COPII), as an interaction partner of the HBV envelope S domain. To understand how HBV co-opts COPII as a proviral machinery, we studied roles of key Sec proteins in HBV-expressing liver cells. Silencing of Sar1, Sec23, and Sec24, which promote COPII assembly conco…

Hepatitis B virusImmunology610 MedizinVesicular Transport ProteinsBiologymedicine.disease_causeProteomicsEndoplasmic ReticulumMicrobiologyCell Line03 medical and health sciencesDownregulation and upregulationTranscription (biology)610 Medical sciencesVirologyddc:570medicineGene silencingHumansProtein IsoformsSecretionRNA Small InterferingCOPII030304 developmental biologyHepatitis B virus0303 health sciences030306 microbiologyEndoplasmic reticulumBiological TransportHepatitis Bdiseases infection microbe–cell interaction proteomics virusesCell biologyHost-Pathogen InteractionsHepatocytesCOP-Coated Vesicles
researchProduct

2014

The hepatitis B virus (HBV) is an enveloped DNA virus that replicates via reverse transcription of its pregenomic RNA (pgRNA). Budding of HBV is supposed to occur at intracellular membranes and requires scission functions of the endosomal sorting complex required for transport (ESCRT) provided by ESCRT-III and VPS4. Here, we have investigated the impact of the upstream-acting ESCRT-I and ESCRT-II complexes in HBV morphogenesis. RNA interference knockdown of the ESCRT-I subunits TSG101 and VPS28 did not block, but rather stimulate virus release. In contrast, RNAi-mediated depletion of the ESCRT-II components EAP20, EAP30 and EAP45 greatly reduced virus egress. By analyzing different steps of…

Hepatitis B virusMultidisciplinaryvirusesRNADNA virusmacromolecular substancesBiologymedicine.disease_causeVirologyVirus ReleaseESCRTCapsidRNA interferenceTranscription (biology)medicinePLOS ONE
researchProduct

Quantitation of HCV-replication using one-step competitive reverse transcription-polymerase chain reaction and a solid phase, colorimetric detection …

1994

A solid phase assay for the colorimetric detection of competitively amplified HCV-cDNA has been established and used to investigate clinical samples from patients with chronic hepatitis. The assay is based on the reduction in the amplification of an hepatitis C virus-related competitor molecule by wild-type hepatitis C virus during polymerase chain reaction. The internal standard contains a lac operator sequence, allowing the amount of amplified competitor to be determined using a lac I-repressor/beta-galactosidase fusion protein. The reduction in the amplification of competitor is dependent upon the concentration of HCV-RNA in the original sample. External hepatitis C virus wild-type stand…

Hepatitis C virusHepacivirusBiologymedicine.disease_causeVirus ReplicationPolymerase Chain ReactionSensitivity and SpecificityViruslaw.inventionFlaviviridaelawmedicineHumansPolymerase chain reactionHepatologyGene AmplificationHepatitis CAmpliconmedicine.diseasebiology.organism_classificationVirologyMolecular biologyHepatitis CReverse transcription polymerase chain reactionTiterRNA ViralColorimetryJournal of hepatology
researchProduct

Clinical evaluation of a single reaction, diagnostic polymerase chain reaction assay for the detection of hepatitis C virus RNA

1996

Abstract Backgrounds/Aims :In the past few years the detection of HCV-RNA by polymerase chain reaction has become a well-established diagnostic tool for patients with chronic hepatitis C. However, the lack of reproducible results between laboratories and the relatively high proportion of false-positive results, has indicated the need for a standardized and reliable polymerase chain reaction assay. In the present study we have analyzed the performance of a commercial, HCV-RNA polymerase chain reaction assay based on a single, combined reverse transcription and amplification reaction and on the use of Uracil-N-glycosilase to prevent carry-over contamination (Amplicor HCV, Roche Molecular Syst…

HepatitisHepatologybiologyHepacivirusHepatitis C virusHepacivirusHepatitis CHepatitis C Antibodiesmedicine.diseasebiology.organism_classificationmedicine.disease_causeHepatitis CPolymerase Chain ReactionVirologyReverse transcriptaselaw.inventionlawmedicineHumansRNA ViralPrimer (molecular biology)Nested polymerase chain reactionPolymerase chain reactionJournal of Hepatology
researchProduct

Immunohistochemical Study as a Tool in Differential Diagnosis of Pediatric Malignant Rhabdoid Tumor

2010

Malignant rhabdoid tumors (MRTs) are aggressive childhood neoplasms, occurring mainly in the kidney and brain. We describe 2 unusual cases of extrarenal and noncranial location (liver and soft tissue with dissemination) mimicking hepatoblastoma, neuroblastoma or Ewing sarcoma. Both cases revealed a polyphenotypic profile, combined with cytokeratin, vimentin, and CD99 expression. INI1/BAF-47 showed negative protein nuclear expression in both cases, suggesting a diagnosis of MRT. An extensive immunohistochemical panel was performed to exclude pediatric tumors reminiscent of MRT. The genetic studies failed to detected MYCN amplification, 11q23 deletion, and EWS break-apart positivity. No alter…

HepatoblastomaPathologymedicine.medical_specialtySkin NeoplasmsHistologyDesmoplastic small-round-cell tumorChromosomal Proteins Non-HistoneCD9912E7 AntigenN-Myc Proto-Oncogene ProteinPathology and Forensic MedicineDiagnosis DifferentialNeoplasms Multiple PrimaryFatal OutcomeAntigens CDNeuroblastomaAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansVimentinRhabdoid TumorChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene Proteinbusiness.industryLiver NeoplasmsInfant NewbornInfantNuclear ProteinsWilms' tumorSMARCB1 Proteinmedicine.diseaseImmunohistochemistryDNA-Binding ProteinsMedical Laboratory TechnologyDrug Resistance NeoplasmKeratinsFemaleSarcomaRNA-Binding Protein EWSDifferential diagnosisbusinessCell Adhesion MoleculesTranscription FactorsApplied Immunohistochemistry & Molecular Morphology
researchProduct

The human liver fatty acid binding protein (FABP1) gene is activated by FOXA1 and PPARα; and repressed by C/EBPα: Implications in FABP1 down-regulati…

2013

Liver fatty acid binding protein (FABP1) prevents lipotoxicity of free fatty acids and regulates fatty acid trafficking and partition. Our objective is to investigate the transcription factors controlling the human FABP1 gene and their regulation in nonalcoholic fatty liver disease (NAFLD). Adenovirus-mediated expression of multiple transcription factors in HepG2 cells and cultured human hepatocytes demonstrated that FOXA1 and PPARα are among the most effective activators of human FABP1, whereas C/EBPα is a major dominant repressor. Moreover, FOXA1 and PPARα induced re-distribution of FABP1 protein and increased cytoplasmic expression. Reporter assays demonstrated that the major basal activ…

Hepatocyte Nuclear Factor 3-alphaMaleRepressorBiologyFatty Acid-Binding ProteinsFatty acid-binding proteinMiceTransactivationNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCCAAT-Enhancer-Binding Protein-alphamedicineAnimalsHumansPPAR alphaadipocyte protein 2Molecular BiologyTranscription factorCells Culturedchemistry.chemical_classificationFatty acidHep G2 CellsCell Biologymedicine.diseaseMolecular biologyFatty LiverMice Inbred C57BLLipotoxicitychemistrybiology.proteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
researchProduct