Publication Date

1-1-2011

Document Type

Dissertation/Thesis

First Advisor

Gasser, Kenneth W.

Degree Name

B.S. (Bachelor of Science)

Department

Department of Biological Sciences

Abstract

In the body, secretion is a vital process providing the release of many different and important macromolecular compounds. Using the pancreas as a model secretory organ, research was conducted pertaining to pancreatic exocytosis and the signal transduction system that controls it. The specific focus of the research is to better understand the role of Nck, a ubiquitous adaptor protein, in cytoskeleton reorganization and pancreatic secretion. The goal of the experiments conducted is to prove that upon stimulation of pancreatic acinar cells, Nck recruits to the secretory vesicles. Nck facilitates protein-protein interactions and acts as a regulator of cytoskeletal activation-dependent processes. This work is important as it gives us a better understanding of the mechanism of pancreatic exocytosis and migration of zymogen granules. Exploring the details of this complex puzzle allows researchers and healthcare providers alike to swiftly assess and find solutions to secretory malfunctions that include diabetes, cystic fibrosis, and pathologies associated with Clostriduim infections. As an adapter protein, Nck can interact with many different proteins. It contains binding domains that can attach receptor and non-receptor tyrosine kinases to proteins responsible for the cytoskeletal reorganization. The research demonstrated that it quickly associates with the secretory granules following stimulation of the cells with the physiological hormone cholecystokinin. This in turn provides the necessary mechanism to facilitate cytoskeletal rearrangement and movement of the vesicle inside the pancreatic acinar cell.

Extent

18 pages

Language

eng

Publisher

Northern Illinois University

Rights Statement

In Copyright

Rights Statement 2

NIU theses are protected by copyright. They may be viewed from Huskie Commons for any purpose, but reproduction or distribution in any format is prohibited without the written permission of the authors.

Media Type

Text

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