Eric J. Bennett

This study identifies ZNF598 as a factor resolving translation stress during metabolic adaptation, showing its role in mitochondrial biogenesis and metabolic flexibility.

This paper uses CRISPR-mediated conditional mutagenesis to show BMP/GDF signaling restricts postnatal bone overgrowth by regulating both periosteal and endosteal osteoblasts.

This paper introduces nanogold probes for identifying proteins in live cells and cryo-ET tomograms, enhancing proteome accessibility for electron microscopy.

This study identifies proteostasis as critical for T cell differentiation potential and tumor-infiltrating lymphocyte function, showing that maintaining E3 ubiquitin ligases improves anti-tumor responses.

This study shows that proteasome inhibitors are ineffective in AML due to activation of HSF1 and autophagy, and that combining autophagy and proteasome inhibition effectively kills AML cells.

The paper maps the functional importance of site-specific ubiquitination across the human proteome by analyzing conservation, perturbation, and machine learning scores.

This study identifies mitochondrial-derived double-stranded RNA as a source of RNA stress in aged neurons, which activates the ISR through PKR and contributes to neurodegeneration.

The paper identifies Angel1 as a key factor in non-stop mRNA decay by showing its role in destabilizing mRNAs lacking stop codons.

This study identifies HAPSTR1 as a HUWE1 substrate that facilitates its nuclear localization, thereby regulating stress signaling pathways and cell proliferation.

The paper presents the cryo-EM structure of HUWE1, revealing its modular architecture and its role in degrading cell-fate decision factors.

This study identifies ZNF598 as a key factor in vaccinia virus mRNA translation by modulating ribosome quality control during infection.

The paper identifies USP21 and OTUD3 as deubiquitylating enzymes that counteract ZNF598-mediated ribosomal ubiquitylation, facilitating ribosome-associated quality control.