USP15 Enhances Re-epithelialization Through Deubiquitinating EIF4A1 During Cutaneous Wound Repair
Yixuan Zhao, Xin Huang, Zewei Zhang, Yifan Zhang, Guoyou Zhang, Tao Zan, Qingfeng Li
Abstract
KO mice. Moreover, inhibition of cell migration and proliferation was observed in the USP15-silenced keratinocytes (HaCaTs). Moreover, we revealed for the first time that USP15 could interact with eukaryotic initiation factor 4A-1 (EIF4A1), thereby promoting translational efficacy in keratinocytes, which is essential for keratinocyte proliferation and migration. Conclusively, the USP15-EIF4A1 complex significantly accelerated re-epithelialization in wound healing. These observations helped elucidate the function and mechanisms of USP15 in modulating re-epithelialization in wound healing, providing a promising target for refractory wound treatment.
Topics & Concepts
Wound healingMedicineCell biologyBiologySurgerySignaling Pathways in DiseaseWound Healing and TreatmentsAutophagy in Disease and Therapy