Thesis (M. Phil.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 133-138).

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 243-262).

ARID proteins are highly conserved among eukaryotes and are involved in chromatin remodeling, differentiation and development. The founding member of the ARID3 subfamily, Bright/ARID3A, is an activator of the immunoglobulin heavy chain locus. Bright has been shown to immortalize mouse embryonic fibroblasts and induce malignant transformation when co-expressed with oncogenic Ras. A genomic locus that encodes a gene paralogous to Bright has been identified as Brightlike/ARID3C. In addition to the highly conserved ARID and REKLES domains, Brightlike contains a conserved sumoylation motif. Brightlike orthologous genes have been identified in all vertebrate genomes examined. Its absence from EST databases suggested that it is a rare transcript, and accordingly, its expression in adult mice appears to be restricted to spleen, testes and thymus. Brightlike is also regulated by alternative pre-mRNA splicing, differential subcellular distribution, and post-translational modification by SUMO. The two isoforms of Brightlike appear to have differential expression in lymphocyte populations. Brightlike and Bright bind to the same DNA motif. Unexpectedly, Bright and Brightlike do not form heterocomplexes on DNA nor compete for binding, suggesting they have independent functions in vivo. Brightlike increases the proliferation potential of mouse embryonic fibroblasts and rescues cells from premature senescence, suggestive of a proto-oncogene. / text

The discovery of the crucial intermediates and pathway in the process of the reverse transcription was reported using single-molecule spectroscopy and related techniques including single-molecule fluorescence resonance energy transfer, fluorescence correlation spectroscopy and confocal imaging. Reverse transcription of the HIV-1 RNA genome involves several complex nucleic acid rearrangement steps that are catalyzed by the HIV-1 nucleocapsid protein (NC), including for example, the annealing of the transactivation response (TAR) region of the viral RNA to the complementary region (TAR DNA) in minus-strand strong-stop DNA. In this dissertation, the research focused on elucidating the mechanism of NC-facilitated TAR DNA/RNA annealing. The single molecule spectroscopic measurements reported that the crucial intermediates as well as the mechanistic insight into the annealing of TAR RNA with TAR DNA mediated by viral NC proteins. The data reveal that NC partially melted the secondary structure of TAR DNA (termed the "YTAR") as well as TAR RNA. In the subsequent studies, various short DNA oligonucleotdies were applied to anneal with the TAR to mimic the initial annealing steps. The data support that the YTAR serves as a nucleation center for the annealing to occur through the multiple sites along the TAR structure. Two major nucleation pathways were observed, which are the annealing through the 3'/5' termini, namely "zipper" pathway and the annealing through the hairpin loop region, namely "kissing" pathway. The annealing mechanism was further explored by performing the annealing of wild-type TAR DNA with wild-type TAR RNA in the presence of NC in vitro. The annealing kinetic data suggest that the nucleation of TAR DNA/RNA annealing occurs in an encounter complex form in which one or two DNA/RNA strands in the "Y" form associated with multiple NC molecules. This encounter complex leads to the multiple nucleation complexes, i.e. zipper or kissing intermediates. The data further indicate that although the two complementary strands nucleate at multiple sites, i.e. any single-strand region of TAR, the annealing of two TAR complements occurs through a common mechanism.

Thesis (Ph. D.)--University of Sydney, 2009. / Title from title screen (viewed February 10, 2009). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Molecular and Microbial Biosciences, Faculty of Science. Degree awarded 2009; thesis submitted 2008. Includes bibliographical references. Also available in print form.

Thesis (M.Phil.)--Hong Kong University of Science and Technology, 2008. / Includes bibliographical references (leaves 78-82). Also available in electronic version.

Thesis (Ph. D.)--University of California, San Diego, 1998. / Vita. Includes bibliographical references (p. 122-138).

Thesis (Ph. D.)--Ohio State University, 2007.

Thesis (Ph. D.)--Georgia State University, 2009. / Title from file title page. William H. Nelson, committee chair; Vadym Apalkov, Stuart A. Allison, Douglas Gies, Gary Hastings, committee members. Description based on contents viewed Nov. 5, 2009. Includes bibliographical references.

Thesis (Ph. D.)--Rutgers University, 2007. / "Graduate Program in Toxicology." Includes bibliographical references (p. 115-131).