J. Paul Taylor

This study shows that electrostatic interactions between intrinsically disordered regions drive G3BP1 condensate ageing, with RNA modulating these interactions and delaying dynamic arrest.

This study identifies nsP3-RBP co-condensation as a mechanism alphaviruses use to sustain replication, showing disruption of these condensates can inhibit viral replication.

This study tests antisense oligonucleotides targeting Hnrnph2 in a mouse model, showing reduced Hnrnph2 levels, increased Hnrnph1, and improved phenotypes like seizures and motor function.

This study investigates YFV-induced stress granules, revealing their enrichment in mitochondrial proteins and their role in mitochondrial dysfunction during infection.

This study shows that stress granule formation during FMDV infection is independent of innate immune activation, and that preventing their disassembly reduces viral replication.

The paper identifies TDP-43-dependent molecular cascades in ALS/FTD by integrating multiomic data from iPSC-derived neurons and validates key genes through experimental assays.

This study identifies a point mutation in SRRM2 as a risk factor for ALS, showing it disrupts protein interactions and dysregulates synapse-related genes.

The paper shows that separable interactions in A1-LCD allow tunable metastability of condensates, which can suppress amyloid fibril formation even with ALS mutations.

The paper identifies heterozygous frameshift variants in hnRNPA2B1 causing early-onset oculopharyngeal muscular dystrophy by altering nucleocytoplasmic transport.

This paper creates a mouse model of HNRNPH2-related neurodevelopmental disorder, showing similar symptoms to humans and revealing genetic compensation mechanisms.

The paper characterizes HNRNPA1 mutations in patients with neurodegenerative diseases, showing varied effects on fibrillization, phase separation, and stress granule dynamics.

The paper identifies an enrichment of rare protein-truncating variants in ALS patients, highlighting novel genes like DNAJC7 and known ALS genes such as SOD1, NEK1, and FUS.

The paper shows that CHCHD10S59L causes mitochondrial toxicity in Drosophila and HeLa cells, which can be mitigated by inhibiting TDP-43 mitochondrial translocation or PINK1 kinase activity.

PeCanPIE is a cloud-based platform for annotating and classifying germline variants in pediatric cancer, using ACMG guidelines to rank and classify variants from VCF files.

The paper introduces OptoGranules, a light-inducible system to control stress granule dynamics in cells, showing that persistent stress granule assembly leads to ALS-FTD-like pathology.