Abigail L. Buchwalter

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 shows that emerin loss impairs MyoD-driven differentiation of human iPSCs into skeletal myotubes by affecting PRC2-mediated gene regulation.

The paper identifies sequences affecting emerin's secretory trafficking, showing C-terminal tags and hydrophobic domains influence its lysosomal fate, while an ER retention motif stabilizes it.

The paper shows that the nuclear periphery represses H3K9me2-marked genes and transposons, and its loss disrupts cell fate transitions in mESCs.

The paper shows that LB1 and LAP2β resist cytoskeletal forces to maintain lamin A/C meshwork and nuclear integrity, preventing rupture upon their depletion.

This study investigates how O-GlcNAc modifications influence lamin A tail processing and identifies a potential link between glucose metabolism and lamina biogenesis.

This study models age-linked rDNA hypermethylation in human cells using dCas9-directed DNA methylation and finds no detectable effect on rRNA transcription or cellular growth.

This study introduces proteome birthdating to measure protein age and finds that ubiquitinated proteins are predominantly newly synthesized, with distinct age distributions across cellular pathways.

TRAIL quantifies protein and cell lifetimes across tissues, showing cell division drives non-selective turnover in proliferative tissues while physicochemical features influence turnover in non-proliferative tissues.