Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex.

ABSTRACT: Traumatic brain injury (TBI) remains the leading cause of death and disability worldwide with no existing effective treatment. The early phase after TBI induction triggers numerous molecular cascades to regulate adaptive processes and cortical network activity. Kinases play a particularly prominent role in modifying peptide substrates, which include ion channels, receptors, transcription factors and inflammatory mediators. This study aimed to better understand the post-injury serine/threonine kinome; (1) Which kinases conduct phosphorylation-induced alterations of target peptides following unilateral TBI in mouse cortex? (2) How do these kinases effectuate pathological network hyperexcitability, which has detrimental long-term outcomes? We used a serine/threonine kinase assay at 4 h, 24 h

SUBMITTER: Gallagher C 

PROVIDER: S-EPMC11883073 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature