Michael J. Eck

This paper develops covalent EGFR inhibitors targeting cysteine 775 and 797, showing improved efficacy and resistance delay in osimertinib-resistant models.

This paper uses CRISPR base editing to map chemical-genetic interactions in the MAPK pathway, revealing drug resistance mechanisms and functional hotspots.

The paper investigates MEK inhibitor selectivity across RAF isoforms and develops a covalent ARAF-MEK inhibitor with improved potency.

This study shows that RAF inhibitors paradoxically activate ARAF, BRAF, and CRAF through dimerization, not negative allostery, by using biochemical assays and mass photometry.

The paper identifies O-mannosylation and protein maturation as therapeutic targets in BRAF fusion oncogenesis by showing their necessity for fusion-induced transformation.

This study compares the potency of thirteen RAF inhibitors against ARAF, BRAF, and CRAF isoforms, revealing differences in inhibitor selectivity and mechanism.

This study identifies FGFR alterations in pediatric gliomas, their association with specific histologies, and their response to targeted therapies.

The paper reports the crystal structure of the THEMIS CABIT2 domain, revealing a novel fold with an inserted SH3-like domain and insights into its interaction with GRB2.

This study identifies the Shh-Eya1 regulatory axis as critical for promoting symmetric cell divisions in cerebellar granule cell precursors by coordinating spindle orientation and cell fate determinants.