Jean‐Philippe Fortin

This paper introduces Partita, a high-density CRISPRa platform for comprehensive gene activation studies, demonstrating its utility in identifying cancer dependencies and resistance pathways in vitro and in vivo.

The paper uses a CRISPR/Cas9 screen to identify genes modulating ASO activity, revealing AP1M1 and TBC1D23 as key regulators of endosome-Golgi transport affecting ASO efficacy.

This paper identifies a potent and specific SMARCA2/A4 degrader, G-6599, which works via FBXO22 recruitment and covalent conjugation, offering therapeutic potential.

The paper introduces an enAsCas12a mouse model and associated libraries for efficient gene editing and screening, identifying drug resistance genes and enabling simultaneous gene knockouts and activations.

The paper identifies regulators of inflammatory macrophage states and shows that TNF mRNA m6A modification controls its stability and contributes to disease.

The paper develops a scalable mutagenic base editor platform to identify drug-resistant variants in cancer genomes efficiently.

The paper introduces crisprVerse, a Bioconductor ecosystem for designing and annotating CRISPR gRNAs across multiple technologies and nucleases.

Compartmap infers higher-order chromatin structure from scRNA-seq and scATAC-seq data, matching specialized chromatin capture methods and identifying clinically relevant structural alterations in single cells.

The paper analyzes how multi-target sgRNAs in CRISPR screens introduce biases in essentiality scores and functional networks.

ComBat, an empirical Bayes location-and-scale model from genomics, removes additive and multiplicative scanner effects from regional cortical thickness across 11 scanners while preserving age associations.

This paper shows that diffusion tensor imaging data are site-specific and demonstrates that ComBat effectively harmonizes them while preserving biological variability.