David M. Chenoweth

This paper identifies new TRIDs that target ribosome pockets to increase PTC readthrough, showing some are more potent than ataluren in vitro.

The paper identifies RNA-binding proteins (RBPs) that activate transcription through molecular grammars similar to transcription factors, revealing their role in transcriptional regulation and RNA processing.

This study shows HSV-1 protein ICP4 increases nuclear fluidity to enable condensate formation, supporting viral replication.

This paper introduces a method to control kinase activity with spatiotemporal precision using conditional localization pharmacology, demonstrating its ability to manipulate the cell cycle.

The paper develops peptide-based compartments that can be delivered into cells to sequester targets and degrade them, demonstrating potential for synthetic organelles in cell engineering.

The paper shows that microtubule depolymerization at kinetochores limits spindle elongation rather than moving chromosomes apart during anaphase.

This study shows that overexpressed MAD1 forms phase-separated condensates that drive mitotic slippage by sequestering MAD2 and weakening the mitotic checkpoint.

This study shows that high telomeric SUMO levels promote APB nucleation and enhance ALT efficiency through BLM recruitment and DNA synthesis.

The paper introduces three genetically encoded tools to specifically ablate excitatory and inhibitory synapses using E3 ligase-dependent degradation mechanisms.

The paper investigates how condensate material properties and chromatin heterogeneity influence nuclear condensate growth, revealing two physical mechanisms and a quantitative theory to explain these dynamics.

This study shows SUMO promotes DNA repair protein collaboration for telomere maintenance in ALT cancer cells without PML bodies.

The paper shows that Nup98 nucleoporins use phase separation to mobilize heterochromatic repair sites and exclude Rad51, promoting homologous recombination and genome integrity.

The paper examines how tissue stiffness scales with collagen levels across different tissues and finds sub-linear scaling that aligns with cellularized gels, suggesting contractility-driven strain inhibition of collagen degradation.

This paper investigates how mechanical strain affects collagen degradation in tendon and heart tissues, finding that moderate strains suppress degradation while higher strains do not.