Tight junctions are vital to skin and are disrupted in atopic dermatitis. However, we do not understand the normal mechanisms contributing to tight junction function, making therapies to enhance their activity elusive. EphA2 is a protein involved in tight junction signaling, as its loss decreases function. We suggest that ligand-targeting EphA2 with ephrin-A1 can enhance tight junctions and alleviate the barrier dysfunction of atopic dermatitis.
|Effective start/end date||7/1/17 → 6/30/18|
- Dermatology Foundation (AGREEMENT 03/29/17)