Mathieu Quesnel-Vallières

This study identifies an alternative splicing mechanism in IRF7 that generates a protein isoform with enhanced transcriptional activity, leading to increased resistance to viral infection.

The paper identifies a NRCAM proteoform with skipped microexons as a targetable surface antigen in pHGG and demonstrates its utility in immunotherapy.

The paper identifies an alternatively spliced NT5C2 isoform contributing to chemoresistance in B-ALL by enhancing nucleosidase activity and 6-MP resistance.

The paper identifies mutations and RNA-binding proteins affecting CD19 splicing and CART-19 therapy resistance through high-throughput mutagenesis and mathematical modeling.

The paper shows that alternative splicing contributes to gene disruption in AML, increasing the number of patients with functional gene loss beyond what is detected by mutations alone.

The paper introduces fastGRO, a method for rapid and scalable profiling of nascent RNA, showing it is more comprehensive and scalable than existing techniques.