Pre Core Mutation
Mostrando 1-12 de 19 artigos, teses e dissertações.
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1. Hepatitis B virus genotypes and mutations in the basal core promoter and pre-core/core in chronically infected patients in southern Brazil: a cross-sectional study of HBV genotypes and mutations in chronic carriers
Introduction In Brazil, little data exist regarding the distribution of genotypes in relation to basal core promoter (BCP) and precore/core mutations among chronic hepatitis B virus (HBV) carriers from different regions of the country. The aim of
Rev. Soc. Bras. Med. Trop.. Publicado em: 2014-12
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2. Estudo da distribuição genotípica e de mutações no genoma do vírus da hepatite B, em pacientes co-infectados pelo vírus da hepatite B e HIV, na Casa da AIDS, do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo / Hepatitis B genotype distribution and frequency of resistance mutations in a group of patients co-infected with HIV and hepatitis B virus (HBV) at an AIDS Outpatient Clinic in Sao Paulo
O objetivo deste estudo foi avaliar a distribuição genotípica e mutações no genoma do vírus da hepatite B (VHB) em um grupo de pacientes co-infectados pelo VHB e vírus da imunodeficiência humana (HIV). Foram incluídos pacientes AgHBs +/HIV+ , atendidos em um ambulatório de referência para pacientes infectados pelo HIV, na cidade de São Paulo. Par
Publicado em: 2011
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3. CaracterizaÃÃo genÃtica do vÃrus da hepatite B em Alagoas
Hepatitis B virus (HBV) has been classified into eight genotypes (A to H), with distinct geographical distributions. The divergences between the genotypes have been defined arbitrarily, based on a difference of more than 8% in the virus genome sequence. Naturally variants are found in regions pre-S/S, pre-core/C and P. The mutation of the precore region (G18
Publicado em: 2009
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4. Mutations in the pre-core region of hepatitis B virus serve to enhance the stability of the secondary structure of the pre-genome encapsidation signal.
We conducted a large-scale survey to determine the frequency and clinical significance of mutations in the pre-core region of hepatitis B virus (HBV). Sera from 263 patients with chronic HBV infection were analyzed by direct sequencing of PCR-amplified HBV DNA. Four major missense/nonsense mutations (M) were found: (M1) C-->T at nucleotide position 1856, Pro
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5. Hepatitis B virus with mutations in the core promoter for an e antigen-negative phenotype in carriers with antibody to e antigen.
Hepatitis B virus (HBV) DNA clones were propagated from 57 carriers with antibody to hepatitis B e antigen (HBeAg) and sequenced within nucleotides (nt) 1685 to 1926 including the core promoter (nt 1742 to 1849) and the pre-C region (nt 1814 to 1900). Mutations in the core promoter or those in the pre-C region, or both, were detected in 328 (97.9%) of 335 cl
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6. Point mutation analysis of the Xenopus laevis RNA polymerase I core promoter.
The core region of the Xenopus laevis pre-ribosomal RNA promoter was subjected to point mutation analysis. A total of 27 point mutants within a 78 base pair region from -64 to +14, (relative to the start of transcription at +1), were assayed by oocyte microinjection. The results locate the 3' boundary of the core promoter at +4 and the 5' boundary at between
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7. 5′- and 3′-terminal nucleotides in the FGFR2 ISAR splicing element core have overlapping roles in exon IIIb activation and exon IIIc repression
The cell type-specific, mutually-exclusive alternative splicing of the fibroblast growth factor receptor 2 (FGFR2) pre-mRNA is tightly regulated. A sequence termed ISAR (intronic splicing activator and repressor) has been implicated as an important cis regulatory element in both activation of exon IIIb and repression of exon IIIc splicing in epithelial
Oxford University Press.
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8. Influence of a Putative Intermolecular Interaction between Core and the Pre-S1 Domain of the Large Envelope Protein on Hepatitis B Virus Secretion
Virion release of hepatitis B virus (HBV) from hepatocytes is a tightly regulated event. It is a dogma that only the mature HBV genome is preferentially allowed to export from the intracellular compartment (J. Summers and W. S. Mason, Cell 29:403-415, 1982). Recently, an “immature secretion” phenotype of a highly frequent naturally occurring HBV variant
American Society for Microbiology.
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9. Transcription initiation in vivo without classical transactivators: DNA kinks flanking the core promoter of the housekeeping yeast adenylate kinase gene, AKY2, position nucleosomes and constitutively activate transcription
The housekeeping gene of the major adenylate kinase in Saccharomyces cerevisiae (AKY2, ADK1) is constitutively transcribed at a moderate level. The promoter has been dissected in order to define elements that effect constitutive transcription. Initiation of mRNA synthesis at the AKY2 promoter is shown to be mediated by a non-canonic core promoter, (TA)6. Nuc
Oxford University Press.
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10. Detection of hepatitis B pre-core mutant by allele specific polymerase chain reaction.
AIM: Development of a specific polymerase chain reaction (PCR) assay for detection of the pre-core, stop codon, mutant of hepatitis B virus (HBV). METHODS: PCR primers, specific at the 3'-end for nucleotide 1896 of either the pre-core, stop codon, mutant or wild type HBV, were synthesised using published sequence data. Positive control templates for both typ
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11. SMU-2 and SMU-1, Caenorhabditis elegans Homologs of Mammalian Spliceosome-Associated Proteins RED and fSAP57, Work Together To Affect Splice Site Choice
Mutations in the Caenorhabditis elegans gene smu-2 suppress mec-8 and unc-52 mutations. It has been proposed that MEC-8 regulates the alternative splicing of unc-52 transcripts, which encode the core protein of perlecan, a basement membrane proteoglycan. We show that mutation in smu-2 leads to enhanced accumulation of transcripts that skip exon 17, but not e
American Society for Microbiology.
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12. U1 snRNA is cleaved by RNase III and processed through an Sm site-dependent pathway.
Core snRNP proteins bind snRNA through the conserved Sm site, PuA(U)n>/=3GPu. While yeast U1 snRNA has three matches to the Sm consensus, the U1 3'-terminal Sm site was found to be both necessary and sufficient for U1 function. Mutation of this site inhibited pre-mRNA splicing, blocked cell division and resulted in the accumulation of two 3'-extended forms o