Timothy D. Martin

This paper identifies tissue-specific synthetic lethal dependencies driven by KRAS mutations across different cell lineages, revealing distinct genetic vulnerabilities shaped by the tissue context.

This paper develops an iPSC platform to rapidly generate alpha-synuclein inclusions and investigates their formation, subtypes, and molecular interactions.

The paper describes a method to control CRISPR/Cas9 activity using proteasomal degradation of an anti-CRISPR protein fused to a degradation or shutoff tag.

The paper identifies synthetic lethal genes and networks for MYC overexpression using CRISPR and shRNA screens, finding that disrupting citrate production and transport inhibits MYC-driven tumor growth.