Lars Plate

This study links polygenic scores for QT interval to changes in Kv11.1 protein interactions in hiPSC-CMs, revealing connections between genetic variants and endocytic trafficking mechanisms.

The paper identifies thyroglobulin variants associated with hypothyroidism risk using biobank data and molecular characterization, revealing distinct pathophysiological mechanisms for different variants.

This study evaluates VX-121's efficacy across 232 rare CFTR variants, finding it generally more effective than VX-445 but with one variant showing reduced selectivity.

This study identifies cellular targets of SARS-CoV-2 Macrodomain 1 using a catalytically inactive mutant, revealing its role in host protein folding and interferon suppression.

This study uses DIA proteomics to analyze age-related changes in proteostasis and UPR dynamics in human neurons and mouse glia co-cultures, revealing cell-type-specific aging responses.

This study identifies branch-specific UPR proteomic targets in BRAF-mutant melanoma using DIA LC-MS, revealing differential XBP1s regulation linked to drug tolerance.

The paper identifies SCCPDH as an off-target of VX-445 using a photoaffinity ligand and chemoproteomics, showing metabolic dysregulation and potential clinical implications.

The paper develops an automated SP3-TMT sample preparation workflow for proteomics, showing it matches manual methods in performance while improving throughput, cost, and error reduction.

The paper uses proteomics and computational modeling to analyze CFTR variants, identifying structural vulnerabilities in NBD1 that limit corrector efficacy and suggesting secondary mutations as a therapeutic strategy.

This study investigates how calnexin modulates the expression and pharmacological rescue of CFTR variants using deep mutational scanning, revealing its role in CFTR assembly and variant-specific corrector responses.

The paper identifies proteostasis interactomes of trafficking-deficient KV11.1 variants and shows pharmacological chaperone rescue of proteostasis network alterations in LQTS-associated variants.

This study identifies Malectin as a host factor that promotes coronavirus replication and viral protein biogenesis by interacting with viral nonstructural proteins.

This study benchmarks AlphaMissense's ability to predict pathogenicity of CFTR missense variants using clinical and functional metrics, finding moderate correlations with some outcomes but limited utility for pharmacological response.

This study shows BRWD3 promotes KDM5 degradation, which maintains H3K4 methylation levels by balancing H3K4me1 and H3K4me3.

This study identifies NASP as the critical H3-H4 histone chaperone in the Drosophila embryo, showing that its absence leads to degradation of soluble H3-H4 pools and embryonic defects.

The paper shows that manipulating the UPR pathway can restore brain function and reduce aging-related deficits.

The paper uses Rosetta comparative modeling to generate structural models of ΔF508 CFTR and its variants, revealing how the mutation destabilizes the protein and how drugs like VX-809 stabilize it.

This study shows that forcing dimerization between ATF6f and XBP1s enhances UPR activity, reducing protein aggregation in neurodegenerative disease models.

This study identifies IGF2 as a disease modifier that reduces intracellular protein aggregates by promoting their extracellular disposal in Huntington's disease models.