Download Dissertation Abstract Hepatitis B virus HBV infection causes acute and chronic viral hepatitis, which is also considered to be a major etiological factor in the development of liver cirrhosis and hepatocellular carcinoma HCC.
Virus-encoded proteins can moderately stimulate transcription of many host cellular transcription elements and transregulate gene expression of host hepatocellular proteins, which may be one of the molecular mechanisms of HBV-associated diseases. The HBx protein encoded by X gene comprises of amino acids, with a molecular mass of approximately HBx acts as a transregulator and its transregulatory effects linked to the progression of HCC from different groups remain controversial.
The exact role of HBx in viral replication and pathogenesis has yet to be elucidated. Comprehensive understanding the transregulatory roles of HBx using oligonucleotide DNA microarray and detecting the changes of gene expression simultanously may help partially clarify the molecular mechanism of HBV infection.
First, to study the transregulatory effects of HBx protein, the recombinant expression plasmid pcDNA3. Oligonucleotide DNA microarray and bioinformatics techniques were employed to screen and analyze the differentially expressed mRNAs between the two groups. Among the 21, genes, it was found that genes were differentially expressed, genes were up-regulated and genes were down-regulated.
These might be target genes transregulated by HBx protein, among which some genes encoding proteins were involved in cell cycle regulation, cell apoptosis, cell signal transduction, immune response, energy metabolism, tumor development and metabasis.
These might explain the possible mechanism of HBx protein in vivo. In addition, we discovered some novel genes with unknown function transregulated by HBx and one of these novel genes was named as HBx transactivated protein 11 XTP Second, to investigate the transcriptional regulatory role of HBx protein on the expression of p53 tumor suppression gene, the promoter sequence of the p53tumor suppression gene p53p was identified and the recombinant reporter gene expression plasmid pCAT3-p53p was constructed and transiently transfected and cotransfected with pcDNA3.
Results showed that the p53 promoter could cis-activate the transcription of the CAT gene. The findings indicated that HBx could transcriptionally inhibit the expression of p53 gene, which might be a possible molecular mechanism responsible for the development of HCC.
Third, we investigated the biological functions of XTPll. The full length encoding sequence and promoter region were confirmed by bioinformatics. After transfection, the CAT activity was detected.
The results indicated that the XTPll promoter identified in this study had transcriptional activity and HBx had transactivating effect on XTPll promoter.
After transfection, fluorescent fusion protein could be observed steadily in cell plasma by fluorescent microscope. We expressed successfully XTPll fusion proteins with c-myc tag in yeast cells.
The yeast cells transformed with pGBKT7-XTPll plasmid could grow well on both the synthetic dropout nutrient medium and turned blue on medium containing x-cc-gal, which suggested that the XTPll protein fused to the GAL4 DNA-binding domain functioned as a transcriptional activation domain in yeast.
Taken together, the findings provide theoretical basis and research methods for the molecular biological mechanism on the transregulatory effects of HBx.The full text of this journal can be found in the EBSCOhost ™ and Al Manhal databases.
The journal is now also Indexed in WEB OF SCIENCE. Biography: Dr.
Pathak received his PhD in Radiation Biology from Kalyani University (Kalyani, West Bengal, India). He served as Assistant Professor in the Radiobiology Department of Manipal University (Manipal, Mangalore, Karnataka, India). Disclaimer: This blog post covers only a fraction of what's wrong with "The China Study." In the years since I wrote it, I've added a number of additional articles expanding on this critique and covering a great deal of new material.
Please read my Forks Over Knives review . The QUOROM statement and its evolution into PRISMA. The QUOROM statement, developed in and published in ,8 was conceived as a reporting guidance for authors reporting a meta-analysis of randomised trials.
Since then, much has happened.
Hepatitis B virus and dried blood spots This project will determine the analytical sensitivity and estimate clinical sensitivity of screening using a new immunoassay for hepatitis B core antibody. The Elecsys Anti-HBsAg assay is an in-vitro diagnostic test for the qualitative detection of total antibodies to the core protein of hepatitis B virus in human .
Hepatitis B virus (HBV) infection causes acute and chronic viral hepatitis, which is also considered to be a major etiological factor in the development of liver cirrhosis and hepatocellular carcinoma (HCC).