Julia E. Conrad

The paper identifies cardiomyocyte-specific vulnerabilities to LMNA mutations using saturation mutagenesis in hiPSCs and cardiomyocytes, revealing how lamin polymer disruption leads to disease.

This study identifies an allosteric mechanism in eIF2B that regulates the Integrated Stress Response by showing how eIF2-P binding inhibits eIF2B activity through latch-helix dislocation.

The paper identifies a third mode of IRE1 activation called TRES, triggered by reduced protein influx into the ER, leading to a distinct gene expression program to rebalance ER load.