Honors: All College Participants
Characterization of gene expression, glucose responsiveness, and cell proliferation in a pancreatic beta cell hybridoma cell line stably overexpressing the transcription factor Glis3
Academic Level at Time of Presentation
Senior
Major
Exercise Science
Minor
Biology
List all Project Mentors & Advisor(s)
Dr. Gary ZeRuth
Presentation Format
Oral Presentation
Abstract/Description
The transcription factor Gli-similar 3 (Glis3) is important for the specification of insulin-producing beta cells during development and is required for the production of insulin in the mature pancreas. Genetic variants of Glis3 have been implicated in the development of diabetes, however the precise etiology remains unclear. Over the course of the semester, a series of experiments will be conducted to characterize a pancreatic hybridoma cell line that lacks insulin expression. Stable overexpression of Glis3 restores insulin expression in this cell line. The phenotype of the stable cells will be characterized focusing on gene activation levels, glucose responsiveness, and their ability to proliferate. Collectively, these studies may provide insight into Glis3 function and how dysfunction of Glis3 signaling leads to diabetes.
Location
Classroom 211, Waterfield Library
Start Date
November 2016
End Date
November 2016
Affiliations
Honors Thesis
Characterization of gene expression, glucose responsiveness, and cell proliferation in a pancreatic beta cell hybridoma cell line stably overexpressing the transcription factor Glis3
Classroom 211, Waterfield Library
The transcription factor Gli-similar 3 (Glis3) is important for the specification of insulin-producing beta cells during development and is required for the production of insulin in the mature pancreas. Genetic variants of Glis3 have been implicated in the development of diabetes, however the precise etiology remains unclear. Over the course of the semester, a series of experiments will be conducted to characterize a pancreatic hybridoma cell line that lacks insulin expression. Stable overexpression of Glis3 restores insulin expression in this cell line. The phenotype of the stable cells will be characterized focusing on gene activation levels, glucose responsiveness, and their ability to proliferate. Collectively, these studies may provide insight into Glis3 function and how dysfunction of Glis3 signaling leads to diabetes.