Kaitlin Bryce



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Cystic Fibrosis (CF) is a lung disease caused by a genetic mutation in the human gene cystic fibrosis transmembrane-conductance regulator (CFTR), and those affected by CF are often also affected by CF related diabetes. The goal of this project was to investigate mitogen activated protein kinases (MAPKs) activation in human pancreatic duct epithelial (H6C7) cells in response to epidermal growth factor (EGF) stimulation. H6C7 cells were grown in media supplemented with EGF and bovine pituitary extract. Cells were incubated with 25 ng/ml human EGF for the times 0, 5 and 20 minutes. Cell extracts were analyzed by western blotting using CFTR, phospho-p38 MAPK, and phospho-ERK1/2 antibodies. The western blots were quantified using Image Lab software and the data was statistically analyzed using Graphpad Prism 9. The results showed that H6C7 cells expressed a nonsignificant decrease in CFTR activation following stimulation. There was a significant increase in phospho-p38 MAPK activation, which peaked at 20 minutes. The results also showed phospho-ERK1/2 activation was rapid following EGF stimulation, however, it dramatically reduced after 20 minutes and was not statistically significant. The significance of the p38 MAPK results may prove useful in further research, however more research is needed to fully investigate the effect of EGF stimulation on CFTR expression and MAPK activation in H6C7 cells.


Honors Capstone Research (HCR)


Biological Sciences

College Name

College of Science


Ahmed Lawan

Publication Date


Document Type



Cystic Fibrosis, Cystic Fibrosis Related Diabetes, MAP Kinase Activation, Pancreatic Ductal Cells

MAPK Activation in Pancreatic Ductal Cells Expressing Wild-type CFTR



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