Search for dissertations about: "splicing regulation"
Showing result 1 - 5 of 112 swedish dissertations containing the words splicing regulation.
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1. The balance of splicing : A novel insight into the splicing regulation of high-risk HPV E6 and E7 oncogenes
Abstract : HPV is associated with several cancers. The genome consists of a long control region, early (E1, E2, E4, E5, E6 and E7) and late (L1 and L2) genes. The E6 and E7 proteins prevent cells from entering apoptosis and regulate the cell cycle. A deregulated expression of these can result in malignant transformations. READ MORE
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2. Regulation of adenovirus alternative pre-mRNA splicing : Functional characterization of exonic and intronic splicing enhancer elements
Abstract : Pre-mRNA splicing and alternative pre-mRNA splicing are key regulatory steps controlling geneexpression in higher eukaryotes. The work in this thesis was focused on a characterization of thesignificance of exonic and intronic splicing enhancer elements for pre-mRNA splicing. READ MORE
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3. Viral Strategies to Regulate Transcription and Pre-mRNA Splicing
Abstract : A typical DNA virus encodes for a few key regulatory proteins that modify the host cell biosynthetic machinery to achieve a selective viral gene statement. One such example is illustrated by the adenovirus E4-ORF4 protein, which form an enzymatically active complex with the serine and threonine-specific protein phosphatase 2A (PP2A). READ MORE
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4. Regulation of Human Papillomavirus Type 16 Late L1 mRNA Splicing
Abstract : Human papillomaviruses (HPVs) cause almost half of the human cancers that are attributable to viruses. HPV type 16 is the most carcinogenic type among the HPVs and is detected in 50% of all cervical cancers. HPV-16 infects epithelial cells and HPV-16 gene expression is tightly linked to the differentiation stage of the infected cells. READ MORE
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5. Regulation of Human Papillomavirus Type 16 mRNA Splicing and Polyadenylation
Abstract : Human papillomavirus type 16 (HPV-16) is the major causative agent of cervical cancer. The life cycle of this oncogenic DNA tumour virus is strictly associated with the differentiation program of the infected epithelial cells. Expression of the viral capsid genes L1 and L2 can only be detected in the terminally differentiated epithelial cells. READ MORE