Samuel R. Meier

This paper introduces CRISPR-StAR, an in vivo CRISPR screening platform with improved normalization and analysis tools, showing it can identify tumor suppressor gene effects not observable in vitro.

This paper identifies a splicing signature caused by PRMT5 inhibition in MTAP-deleted cancers, showing histology-agnostic splicing changes and potential as a biomarker for PRMT5 inhibitor activity.

The paper identifies HBS1L as a synthetic lethal target in FOCAD-deleted cancer through combinatorial CRISPR screens and validates its dependency via genetic manipulation and in vivo experiments.

This study functionally tests STK11 missense variants in mammalian cells, identifying pathogenic variants and providing insights for clinical interpretation.

The paper presents a large ASE resource from GTEx v8 with 431 million SNP-level and 153 million haplotype-level measurements, and extends phASER to estimate cis regulatory variant effect sizes.

The paper uses bulk RNA-seq data to estimate cell type abundances and identifies cell type interaction QTLs that provide finer resolution of tissue specificity than bulk cis-eQTLs.

The paper examines telomere length variation across 6,391 tissue samples from 952 individuals, showing tissue-specific differences, positive correlations between tissues, and associations with age and ancestry.

Integrating expression, allelic expression and splicing across tissues identifies rare variants with relevance to traits.

The paper quantifies protein levels across 32 human tissues and compares them to transcriptome data, revealing insights into post-transcriptional regulation and disease mechanisms.