Date of Award
Fall 11-22-2016
Degree Type
Thesis
Degree Name
Master of Science (MS)
Department
Biological Science
First Advisor
Phillip Funk, PhD
Second Advisor
Eric Norstrom, PhD
Third Advisor
David Everly, PhD
Abstract
To effectively eliminate the variety of pathogens that an individual may encounter in their lifetime, the immune system has evolved to recognize many different antigens. Within adaptive immunity there are also safe guards where the self-reactive or defective cells are eliminated (1). The removal of such cells is by apoptosis, which is a form of cell suicide characterized by an orderly breakdown of the cell to limit the leakage of cytoplasmic components that could cause inflammation. Apoptosis can be initiated by signaling through specific cell surface molecules and is carried out by downstream mediators. While several model systems of apoptosis do exist, one pathway in developing avian B-cells, which is activated by the cell surface molecule chB6, has yet to be elucidated(4,5). The Funk lab has been interested in the role of alloantigen chB6 (Bu1) in the developing of B cells within the bursa and has shown that chB6 can trigger apoptosis. When an agonist antibody stimulates chB6, rapid cell death follows and it is presumed that there is an endogenous ligand. Funk lab has evidence which suggests that there is certain section of chB6 molecule that is essential in initiating a death signal inside the cell (Funk unpublished). Within this death signaling region is a SH3 binding site and I was interested in testing whether mutating this SH3 binding site affects the cell death. This project furthers our understanding of the biology of chB6.
Recommended Citation
Bhattacharya, Rohini, "Mutagenic Analysis of SH3 Binding Site in the Avian ChB6 Alloantigen" (2016). College of Science and Health Theses and Dissertations. 200.
https://via.library.depaul.edu/csh_etd/200
SLP Collection
no