Thesis (Ph.D.). / Written for the Dept. of Biology. Title from title page of PDF (viewed 2008/02/12). Includes bibliographical references.

Thesis (Ph. D.)--School of Pharmacy and School of Dentistry. University of Missouri--Kansas City, 1998. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [106]-127).

Integrin recycling has been generally assumed to be important for cell migration but the trafficking pathways and the molecules regulating integrin trafficking remain poorly characterized. Furthermore, little is known about the activation status of endocytosed integrins and how it affects the recycling of these receptors. It is likely that FA-engaged integrins will follow different trafficking pathways than bulk integrins and here I sought to study the endocytic fate of this particular integrin pool using the MT-induced FA disassembly assay. I found that integrins previously resident at FAs travel through different Rab compartments after FA disassembly and that their return to the plasma membrane is Rab11- and Src-dependent. Strikingly, I unveiled new functions for FAK and Src family kinases in this process by showing that these kinases are critical to keep integrins active during endocytic trafficking. This finding is unprecedented since it was not known whether endocytosed integrins were kept active during their trafficking. Interestingly, reassembly of FAs from endocytosed integrin occurred preferentially at the leading edge of migrating cells suggesting that integrins are trafficked in a polarized fashion. Furthermore, the recycling of integrins from the Rab11-positive compartment to the plasma membrane is a long-range transport implying the existence of a MT motor committed to this task. Consistently, I identified that a kinesin-II motor, Kif3AC, is engaged in this process. My work establishes a FAK- and Src family kinases-based mechanism for integrin "adhesion memory" during endocytic trafficking and identifies a direct link between FA disassembly and reassembly through an endocytic recycling pathway involving Rab5 and Rab11 and a kinesin-II family member.

Abstract not available

Bibliography: leaves 250-284. / xviii, 284 leaves : ill., plates (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, School of Molecular and Biomedical Science, Discipline of Microbiology and Immunology, 2004

Thesis (Ph. D. in Cancer Biology)--Vanderbilt University, May 2007. / Title from title screen. Includes bibliographical references.

No description available.

Cadherin and catenin-family proteins regulate adhesion in malignant melanoma. Using AQUA (Automated Quantitative Analysis) to quantitate the levels of alpha-catenin, beta-catenin, p120-catenin, N-cadherin, E-cadherin, and P-cadherin in melanoma on tissue microarrays (TMAs), we classified 513 patients by protein expression using hierarchical clustering and regression analysis. The dendrogram supported positive correlations seen upon Spearman rho analysis of P-cadherin and beta-catenin (r=0.5238, p<0.0001) and negative, weak association of N-cadherin with other markers. Patients with high expression of N-cadherin had the highest 20-year survival rate (p=0.0003). Our adherens protein molecular classification of melanoma defines at least two distinctive sub-populations of melanoma patients, those with high expression of N-cadherin and those with low expression who have decreased survival. These findings extend previous cDNA array-based findings of an epithelioid class and neural crest class of melanomas.

Thesis (M.S. in Bio. E.)--School of Biomedical Engineering, Georgia Institute of Technology, 2004. Directed by Cheng Zhu. / Includes bibliographical references (leaves 79-84).