Sara Picó

The paper demonstrates that splice-switching antisense oligonucleotides (SSOs) targeting the downstream splice acceptor site of a microexon can modulate microexon inclusion and restore protein levels of ASD risk genes.

This study shows that loss of H3K9me3 in adult mice leads to premature aging, characterized by reduced lifespan, frailty, and accelerated epigenetic aging.

This study shows that partial reprogramming of dentate gyrus neurons in mice improves memory and learning in aged animals.

This study induces in vivo reprogramming in C. elegans and finds it leads to heterogeneous effects on lifespan depending on developmental stage.

This study compares mouse strains for in vivo reprogramming to develop safer strategies and create a comprehensive atlas of reprogrammable strains.

The paper compares DNA methylation age in four premature aging mouse models, finding ERCC1 mice show the most significant increase in epigenetic age.

This study shows that continuous in vivo reprogramming with OSKM causes hepatic and intestinal failure, leading to premature death, but a new mouse strain reduces these effects.

This study identifies aberrant CPEB4 splicing and downstream mis-expression of SCZ-risk genes as a novel etiological mechanism in schizophrenia.