Thesis (M.S.)--University of Missouri-Columbia, 2003. / Figure 1 referred to on leaf 2 is shown on leaf 20. Typescript. Includes bibliographical references (leaves 35-36). Also available on the Internet.

Due to their role in cellular signaling, mitogen activated protein (MAP) kinases represent targets of pharmaceutical interest. Most MAP kinase inhibitors target the highly conserved ATP binding site. This conservation promotes cross-reactivity and toxicities that may limit their potential as drugs. These drawbacks motivate the search for non-ATP competitive inhibitors with acceptable specificity and potency and also drive efforts to understand MAPK regulation. We applied a virtual screening (VS) workflow to discover novel scaffolds for ATP-independent JNK (C-Jun N-terminal Kinase) inhibitors targeting the JNK-JIP (JNK Interacting Protein) interaction. (-)-Zuonin A was identified as an inhibitor of JNK, exhibiting 100-fold selectivity for the JNKs over other MAP kinases. (-)-Zuonin A was characterized extensively both in vitro and in cell-based assays. The JNK2 isoform has been reported to regulate breast cancer cell migration. Accordingly, we engineered a JNK2-selective peptide inhibitor. Peptides derived from the JIP scaffolds linked to the cell-penetrating peptide TAT are used widely to investigate JNK-mediated signaling events without exibiiting isoform selectivity. Herein, Several JIP-based peptide sequences were designed and tested. A JIP sequence connected through a flexible linker to either the N-terminus of an inverted TAT sequence [mathematical equation], or to a poly-arginine sequence [mathematical equation] enabled the potent inhibition of JNK2 (IC₅₀~90 nM) with 10-fold selectivity over JNK1 and JNK3. Both peptides revealed a potent ability to inhibit the induction of JNK activation and c-Jun phosphorylation in HEK293 cells treated with anisomycin, and inhibited the migration of Polyoma Middle-T Antigen Mammary Tumor (P[subscript y]VMT) cells through the selective inhibition of JNK2. ERK2 dimerization has been reported to regulate its nuclear translocation and signaling. Our analysis using light scattering, analytical ultracentrifugation and NMR provide strong evidence that ERK2 is monomeric under physiological conditions. / text

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An independent S design employing a distractor-type task was used to investigate release from proactive inhibition (PI) as a function of intertrial interval (ITI) in short-term memory (STM). Of specific interest was whether PI release was provided by shift in ITI length rather than a function of lengthening the ITI. Four groups were employed in this study. One group received short ITIs for 4 trials and then a long ITI for the next 2 trials; another group shifted from a long to short ITI, and two additional groups received constant ITIs throughout. It was found that neither lengthening ITI nor a shift in ITI length provided a release from PI. Implications concerning time as an organizational (clustering) factor in final recall were not substantiated.

Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 4 uppsatser.

Zugl.: Berlin, Humboldt-Univ., Diss., 2007

Thesis (Ph. D.)--Columbia University, 1923. / Vita. "Reprinted from Archives of psychology, no. 63."

Thesis (Ph. D.)--Catholic University of America, 1939. / Vita. Bibliography: p. 41-42.

Thesis (Ph. D.)--York University, 2003. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves 189-205). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pNQ82806.