FTO promotes post-stroke neuroprotection by m⁶A demethylation of c-Jun.

ABSTRACT: N⁶-methyladenosine (m⁶A) is a critical epitranscriptomic regulator of neuronal function. Cerebral ischemia induces m⁶A hypermethylation due to decreased expression of m⁶A demethylase fat mass and obesity-associated (FTO) protein. Previously, we showed that cerebral overexpression of FTO with an adeno-associated virus (AAV) 9 protects the post-stroke brain. We presently evaluated the mechanistic basis for FTO-dependent m⁶A demethylation in post-ischemic neuroprotection using the mice transient middle cerebral artery occlusion model of experimental stroke. Based on the bioinformatic predictions and m⁶A abundance, pro-apoptotic transcription factor Jun proto-oncogene (c-Jun) with 19 m⁶A sites was chosen as an

SUBMITTER: Chokkalla AK 

PROVIDER: S-EPMC12081378 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature