J. Wade Harper

The paper develops GolgiFold, a structure-based PPI map of human Golgi proteins, identifying over 1,800 interactions and confirming new protein contacts through experimental validation.

The paper identifies a cell-state-dependent pathway for degrading ER-retained 60S ribosomal subunits through UFMylation loss and the action of TLSD1.

This study identifies BAF complex interaction with FOS in regulating ASD-associated gene programs through enhancer activation and shows how genetic variants disrupt this process.

In S. japonicus, the ESCRT adaptor Alx1 activates the essential PH-domain protein Vid27 through interaction, driving postmitotic nuclear envelope sealing independently of Cmp7 and ESCRT-III.

Cryo-EM at 2.4 Å shows DNAJC13 as an antiparallel arch-shaped homodimer with a buried InsP6 pocket; dimerization controls WASH recruitment, tubule fission, and melanin production.

The paper develops a human stem cell toolkit for studying lysosomal storage disorders by generating proteomic data from induced cortical and dopaminergic-like neurons.

This study reveals how FBXO7 and PI31 regulate the proteasome 20S core particle and how disease variants disrupt this function.

The paper shows that LD-targeted proteins are confined by nanodomains and transported via ER-LD bridges, revealing mechanisms for their selective accumulation on lipid droplets.

This study shows that LLOMe forms amyloid structures inside lysosomes that mechanically rupture the lysosomal membrane, revealing a structural mechanism for lysosomal damage.

This paper uses machine learning to predict high-affinity nanobody binders from sparse sequencing data, outperforming deep learning and semi-supervised methods with linear models.

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

This study shows that alpha-synuclein fibrils sequester and degrade ESCRT-III proteins, leading to endolysosomal damage and increased alpha-synuclein aggregation.

The paper creates a structural interactome of human endosomes using cross-linking, mass spectrometry, and AlphaFold, identifying structural models for endosomal protein complexes.

This study uses nMOST to profile proteo-lipidomics in lysosomal storage disease mutants, revealing autophagy defects and mitochondrial dysfunction.

This study identifies UBE3C and NRF1-dependent proteasomal pathways that regulate acute protein aggregate turnover in response to misfolded protein accumulation.

This paper develops Endo-IP and Lyso-IP methods to profile endolysosomal proteins in induced neurons, revealing cargo and machinery involved in neurodegenerative disease.

This study profiles proteomic changes in subcellular compartments during NLRP3 inflammasome activation and identifies disruptions in retrograde trafficking pathways.

The paper uses cryo-EM to visualize the assembly of the human 20S proteasome, revealing how chaperones and propeptides guide subunit incorporation and proteasome activation.

The paper uses ER stressors in ALS patient-derived motor neurons to identify druggable targets that protect against degeneration.

This study identifies MTK458, a PINK1 activator, which reduces α-synuclein pathology and pUb levels in Parkinson's disease models and correlates plasma pUb with disease progression.

The paper uses proteomics to compare autophagy cargos in two Parkinson disease mouse models, finding distinct adaptive pathways in PINK1 and LRRK2 models.

This study investigates how the 22q11.2 deletion affects gene expression in neural progenitor cells and neurons, linking it to schizophrenia risk through altered presynaptic gene products.

The paper integrates protein imaging and interaction data to create a unified map of eukaryotic cell structure, revealing new subcellular systems and protein associations.

The paper creates two large-scale cell-line-specific human interactomes using affinity-purification mass spectrometry and identifies shared and cell-specific protein interactions.