C. Jane McGlade

This study demonstrates that activating CBL ubiquitin ligase via engineered mutants or small molecules can downregulate tyrosine kinase signaling by enhancing substrate ubiquitination and reducing downstream signaling.

This study identifies SRRM1 as a splicing regulator that promotes oncogenic NUMB isoforms and other cancer-related splicing events, leading to increased tumorigenic properties in multiple cancer cell lines.

The paper shows that high NUMB exon 9 inclusion in tumors is linked to immune evasion and metabolic changes that support tumor growth.

The paper analyzes human NUMB alternative splicing across tissues using RNA-seq data to show tissue-specific isoform expression patterns.

This study identifies how SLAP2 binding to CBL disrupts its autoinhibition, revealing a mechanism for activating CBL's ubiquitin ligase function.