Thesis (Ph. D.) -- University of Texas Southwestern Medical Center at Dallas, 2003. / Vita. Bibliography: 160-180.

Thesis (Ph.D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 11, 2009) Includes bibliographical references.

Thesis (PhD)--Montana State University--Bozeman, 2008. / Typescript. Chairperson, Graduate Committee: Michele Hardy. Includes bibliographical references (leaves 141-173).

Thesis (M. S.)--Biology, Georgia Institute of Technology, 2006. / Jung Choi, Committee Member ; Yury Chernoff, Committee Chair ; kirill.lobachev@biology.gatech.edu, Committee Member.

Thesis (M.S.)--West Virginia University, 2010. / Title from document title page. Document formatted into pages; contains v, 46 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 43-46).

Würzburg, Univ., Diss., 2001.

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Universiẗat, Diss., 2002--Bayreuth. / Erscheinungsjahr an der Haupttitelstelle: 2002.

Thesis (Ph. D.)--University of Chicago, Dept. of Biochemistry and Molecular Biology, March 2001. / Includes bibliographical references. Also available on the Internet.

Fbxl13 (F-box and leucine-rich repeat protein 13) is an orphan F-box protein. Fbox proteins are a family of substrate-targeting specificity factors for the SCF superfamily of E3 ubiquitin ligases. Since their discovery, many F-box proteins have been shown to have oncogenic and tumour suppressive roles. The importance of Fbxl13 itself in tumourigenesis is reflected in several genome-wide shRNA screens. Fbxl13 depletion in human cancer cells correlates with increased ionising radiation sensitivity and increased genomic instability. Furthermore, Fbxl13 depletion reduces proliferation in mouse embryonic epidermis. Conversely, Fbxl13 amplification is frequently observed in several cancer patient cohorts. However, the main function of Fbxl13 is unknown and its biochemical mechanism of action remains uncharacterised. The aim of this study was to identify the interactors, substrates, and functions of Fbxl13, in order to elucidate its role in tumourigenesis. In this study, I identify and validate Fbxl13 interactors Centrin-2, Centrin-3, Cep152, and Cep192. I show that Fbxl13 is enriched at the centrosome, and present evidence that Fbxl13 targets Cep192-3 for ubiquitin mediated proteolysis. In line with this, Fbxl13 overexpression downregulated centrosomal Cep192 and γ-tubulin, and disrupted the microtubule nucleation activity at the centrosome. Finally, Fbxl13 amplification in U2OS cells is associated with increased cell motility. Thus, we propose that Fbxl13 is a novel regulator of centrosome microtubule nucleation activity.