Etk/Bmx is a member of the Tec family protein kinases which are mainly expressed in epithelial and endothelial cells. Tec family protein kinases are important regulators of signal transduction for activation of cell growth, differentiation and development. Current information on Etk/Bmx’s functions in traumatic brain injury (TBI) shows a significant involvement of this Tec kinase. Correlation of Etk/Bmx to severity of TBI has been demonstrated in rat models, and its single nucleotide polymorphism is associated with clinical presentations of post-TBI dizziness. Etk/Bmx had been implicated as a chronic inflammation mediator in scar formation and also demonstrated its potential as a biomarker in TBI. With these recent findings, we speculate that another role of Etk is a therapeutic target or mediator of symptoms for TBI. The mechanisms behind the role of Etk/Bmx in TBI are not yet understood completely. Further investigation of the mechanisms and roles of Etk/Bmx in TBI is necessary to confirm the potential of Etk/Bmx as a novel therapeutic target or mediator of symptoms for TBI. In this study, we aim to (1) investigate the genomic regulatons of Etk/Bmx involved in TBI; (2) investigate the epigenomic modifications of Etk/Bmx and its promoter after TBI; (3) identify phosphorylation sites of Etk/Bmx and assess its role in treatment of TBI.
|Effective start/end date||8/1/15 → 7/31/16|
- Traumatic brain injury