Breaking down barriers: defining the role of EphA2 in building epidermal tight junctions

Project: Research project

Description

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.
StatusFinished
Effective start/end date7/1/176/30/18

Funding

  • Dermatology Foundation (AGREEMENT 03/29/17)

Fingerprint

Tight Junctions
Atopic Dermatitis
Ephrin-A1
Ligands
Skin
Proteins
Therapeutics