Investigation of Fringe protein modulation of osteoclast differentiation and activity
Faculty Mentor
Jason Ashley
Presentation Type
Poster
Start Date
4-14-2026 9:00 AM
End Date
4-14-2026 11:00 AM
Location
PUB NCR
Primary Discipline of Presentation
Biology
Abstract
Osteoporosis, a prevalent low bone density disorder typical of advanced aging, is driven by the overactivation and prolonged survival of osteoclast cells responsible for the resorption of bone tissue. Osteoclasts are therefore common targets of antiresorptive therapies to treat osteoporosis. However, limitations in therapies that either have poor side effects or short efficacy windows warrant the investigation of undiscovered mechanisms underlying the biology of osteoclasts that may reveal novel targets for emerging therapeutics. Notch receptors, which are transmembrane proteins that participate in direct contact signaling with ligands embedded in the membrane of adjacent cells, have long been understood to influence osteoclast differentiation and activity. Additionally, Fringe proteins, a family of three N-acetylglucosamine transferases (called Lunatic, Manic, and Radical) that each uniquely extend covalently linked sugars on epidermal growth factor repeats located on the Notch receptor extracellular domain, are known to modulate the strength of Notch signaling and alter how cells respond to Notch. All three Fringe proteins are known to be expressed during osteoclast differentiation, but at different levels. Lunatic Fringe, for example, is expressed much higher than Manic or Radical. We are therefore investigating the role of Notch activation of osteoclasts under altered Fringe protein expression. Specifically, we aim to determine how each Fringe protein uniquely contributes to osteoclast differentiation and activity by knocking them out one at a time in osteoclast precursors and assessing how their absence modulates osteoclast behavior.
Recommended Citation
Purdue, Stephen, "Investigation of Fringe protein modulation of osteoclast differentiation and activity" (2026). 2026 Symposium. 24.
https://dc.ewu.edu/srcw_2026/ps_2026/p1_2026/24
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Investigation of Fringe protein modulation of osteoclast differentiation and activity
PUB NCR
Osteoporosis, a prevalent low bone density disorder typical of advanced aging, is driven by the overactivation and prolonged survival of osteoclast cells responsible for the resorption of bone tissue. Osteoclasts are therefore common targets of antiresorptive therapies to treat osteoporosis. However, limitations in therapies that either have poor side effects or short efficacy windows warrant the investigation of undiscovered mechanisms underlying the biology of osteoclasts that may reveal novel targets for emerging therapeutics. Notch receptors, which are transmembrane proteins that participate in direct contact signaling with ligands embedded in the membrane of adjacent cells, have long been understood to influence osteoclast differentiation and activity. Additionally, Fringe proteins, a family of three N-acetylglucosamine transferases (called Lunatic, Manic, and Radical) that each uniquely extend covalently linked sugars on epidermal growth factor repeats located on the Notch receptor extracellular domain, are known to modulate the strength of Notch signaling and alter how cells respond to Notch. All three Fringe proteins are known to be expressed during osteoclast differentiation, but at different levels. Lunatic Fringe, for example, is expressed much higher than Manic or Radical. We are therefore investigating the role of Notch activation of osteoclasts under altered Fringe protein expression. Specifically, we aim to determine how each Fringe protein uniquely contributes to osteoclast differentiation and activity by knocking them out one at a time in osteoclast precursors and assessing how their absence modulates osteoclast behavior.
