Stephen Joseph Elledge

The paper identifies two proteasomal mechanisms that target proteins with exposed cysteines, revealing their role in quality control and linking them to human diseases.

This paper identifies tissue-specific synthetic lethal dependencies driven by KRAS mutations across different cell lineages, revealing distinct genetic vulnerabilities shaped by the tissue context.

A >50,000-element viral smORF library screened by growth, MHC-I, ER stress, Perturb-seq and mass spectrometry yields >2,000 active microproteins and shows EBV BNLF2b inhibits PKA by mimicry.

This study identifies germline-encoded features as the primary driver of immunodominance in antibody responses to SARS-CoV-2, using structural modeling and mutational analysis.

The paper identifies C-terminal degron substrates of the CTLH E3 ligase complex and links their regulation to ribosome biogenesis through the chaperone activity of AAMP.

The paper reports the cryo-EM structure of TXNL1-bound proteasome and identifies interactions critical for stress-induced degradation of TXNL1.

The paper replicates a 2005 finding that BRIT1/MCPH1 is essential for G2/M checkpoint activation in response to DNA damage, confirming the original conclusion after identifying and correcting a figure duplication error.

This study reveals the structural basis of the midnolin-proteasome pathway and shows that midnolin downregulation promotes myeloma cell survival by enhancing IRF4 expression.

This paper describes a novel RNA splicing system, SOS splicing, that removes transposons from mRNAs in C. elegans and human cells, protecting genes from TE-mediated disruption.

This paper uses GPT-4 to automate curation of E3-substrate relationships from literature, resulting in a database of 3,294 pairs with high accuracy.

This study identifies metabolic vulnerabilities in aneuploid cancer cells through CRISPR screens and multi-omic analysis, revealing reliance on pyrimidine biosynthesis and sensitivity to DNA-damaging drugs.

This paper develops an iPSC platform to rapidly generate alpha-synuclein inclusions and investigates their formation, subtypes, and molecular interactions.

This study identifies a synergistic effect between AKT inhibitors and pitavastatin in killing triple-negative breast cancer cells by targeting cholesterol trafficking.

The paper describes a method to control CRISPR/Cas9 activity using proteasomal degradation of an anti-CRISPR protein fused to a degradation or shutoff tag.

The paper identifies synthetic lethal genes and networks for MYC overexpression using CRISPR and shRNA screens, finding that disrupting citrate production and transport inhibits MYC-driven tumor growth.

This study identifies KIAA1841 as a negative regulator of class switch recombination in B cells through a shRNA screen in mouse B cell lines.