Thesis (Ph. D.)--University of Virginia, 2006. / Includes bibliographical references. Also available online through Digital Dissertations.

Thesis (Ph. D.)--Cornell University, January, 2007. / Vita. Includes bibliographical references (leaves 204-240).

Thesis (Ph. D.)--University of Toledo, 2008. / Typescript. "Submitted as partial fulfillment of the requirements for the Doctor of Philosophy in Chemistry." Includes bibliographical references (leaves 305-309).

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 91-109).

Thesis (M.S.)--Rutgers University, 2009. / "Graduate Program in Chemical and Biochemical Engineering." Includes bibliographical references (p. 55-58).

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 82-95).

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 79-94).

Thesis (Ph. D.)--University of California, Riverside, 2009. / Includes abstract. Title from first page of PDF file (viewed March 8, 2010). Includes bibliographical references. Issued in print and online. Available via ProQuest Digital Dissertations.

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

abstract / Pharmacology and Pharmacy / Doctoral / Doctor of Philosophy