Tight Junction Protein Impact on Sonic Hedgehog Pathway

Authors

Josh Freeman, Brigham Young University - ProvoFollow
Hudson Christensen, Brigham Young University - Provo
Dario Mizrachi, Brigham Young University - ProvoFollow

Files

Keywords

Chimera Occludin. SMO upregulation. GLI transcription Factors

Abstract

The Sonic Hedgehog Pathway is critical for cell division and proliferation, and when disrupted, can be a major contributor to the overproliferation of cells and complications in the organism from the resultant cancers. Experimentation upon the organism Planaria Torva and A549 cells using chimera Occludin (COC)–a traditionally isolated tight junction protein having no role in the SHH pathway–has shown dramatic changes within the organism/cell signaling system, suggesting that tight-junction proteins may play a role in–or can be used to manipulate–this specific cell signaling pathway by inhibiting or activating key proteins. The possibility of a “mechanotransduction” effect by COC on SHH pathway has major implications regarding our understanding of the physiological pathways related to cancer, as well as its research and treatment.

BYU ScholarsArchive Citation

Freeman, Josh; Christensen, Hudson; and Mizrachi, Dario, "Tight Junction Protein Impact on Sonic Hedgehog Pathway" (2025). Library/Life Sciences Undergraduate Poster Competition 2025. 5.
https://scholarsarchive.byu.edu/library_studentposters_2025/5

Document Type

Book

Publication Date

2025

Language

English

College

Life Sciences

Department

Cell Biology and Physiology

University Standing at Time of Publication

Junior

Copyright Use Information

https://lib.byu.edu/about/copyright/