METTL3-IGF2BP3 m⁶A axis drives mutant huntingtin stability and neurodegeneration in Huntington’s disease
This study identifies the METTL3-IGF2BP3 m⁶A axis as a critical driver of mutant huntingtin accumulation and neurodegeneration in Huntington's disease, demonstrating that targeting this epitranscriptomic pathway selectively reduces mHTT toxicity and inflammation in affected cells.