Global ETD Search

1	Autosomal dominant polycystic kidney disease : biochemical studies of polycystin-1, the product of the human PKD1-gene Weston, Benjamin Saul January 1999 (has links) No description available. 572 Cysts; Fusion proteins
2	Analysis of the utilisation of second ORFs in pneumovirus mRNA Baghbadorani, G. Ahmadian January 1998 (has links) No description available. 572.8 Fusion proteins
3	Antibody-guided enzyme nitrile therapy of cancer Kousparou, Christina January 2000 (has links) No description available. 572 Fusion; Proteins
4	The cloning and subcellular localisation of maize streak virus ORF V1 Dickinson, Victoria Jane January 1996 (has links) No description available. 579 Fusion proteins
5	Production of recombinant enzyme-antibody conjugates for use in cancer chemotherapy Michael, Nigel Paul January 1996 (has links) No description available. 572.8 Fusion proteins; Molecular cloning
6	Studies on the mechanism of protein kinase C down-regulation Smart, Nicola January 1999 (has links) No description available. 572
7	Tissue transglutaminase : a new secretory protein Gaudrey, Claire Anne January 1998 (has links) No description available. 572
8	Trans-dominant negative inhibition of human immunodeficiency virus type 1 replication by expression of protease-reverse transcriptase fusion proteins Cherry, Elana. January 1999 (has links) No description available. HIV-1. Viral Fusion Proteins. Protease Inhibitors.
9	Trans-dominant negative inhibition of human immunodeficiency virus type 1 replication by expression of protease-reverse transcriptase fusion proteins Cherry, Elana. January 1999 (has links) The molecular mechanisms involved in the regulation of protease (PR) activity and human immunodeficiency virus type 1 (HIV-1) viral maturation are incompletely elucidated. To better understand the importance of the cleavage event between HIV-1 PR and reverse transcriptase (RT), we have selectively mutagenized specific residues at the junction between these genes to produce a PR-RT fusion protein in the context of a full-length proviral construct. Mutant viruses derived from COS-7 cells transfected with this construct were analyzed in regard to each of viral replication, maturation, and infectivity. Immunoblot analysis revealed that the mutation prevented cleavage between the PR and RT proteins and that both existed as a PR:RT fusion protein in each of cellular and viral lysates. Interestingly, intracellular PR that existed within the PR-RT fusion protein not only remained functionally active, bid also processed HIV-1 precursor proteins with slightly increased efficiency as shown in time-course experiments in transfected COS-7 cells. In contrast, the RT component of the fusion protein was active at wild-type levels in in vitro and endogenous RT assays. Electron microscopy revealed that mutant viruses containing the cleavage site mutation between PR and RT possessed wild-type morphology. These viruses also displayed wild-type sensitivities to inhibitors of each of HIV-1 PR and RT activities. However, viruses containing the PR-RT fusion protein were 20-times less infectious than Wild-type viruses. This defect was further pronounced when mutated Gag-Pol proteins were overexpressed as a consequence of an additional mutation that interfered with frameshifting. Thus, unlike cleavage site mutations at the N-terminus of PR, a cleavage site mutation between PR and RT did not prevent proteolytic processing and abolish infectivity; rather, viruses containing PRAT fusion proteins were viable, in agreement with the notion that C-terminal liberation of PR is not as critical for HIV-1. Protease Inhibitors. Viral Fusion Proteins.
10	Structural studies on strain X:31 influenza hemagglutinin / Gray, Cameron. January 1998 (has links) Thesis (Ph. D.)--University of Virginia, 1998. / Includes bibliographical references (p. 163-177). Also available online through Digital Dissertations.

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