J. P. Taylor

The paper shows that the mitochondrial unfolded protein response (UPRmt) interacts with stress granules (SGs) to regulate cellular stress responses and mitochondrial homeostasis.

This study identifies the role of G3BP1-N interaction in SARS-CoV-2 replication by showing that disrupting this interaction reduces viral replication and pathogenesis.

This study identifies two small molecules that inhibit G3BP-driven stress granule formation and dissolve pre-existing granules, showing broad efficacy across cell types and stressors.

TransitID maps proteome trafficking between cellular compartments and between cells with nanometer resolution, revealing new roles for stress granules and intercellular signaling.

This study identifies a new Karyopherin-β2 binding epitope in HNRNPH2 linked to neurodevelopmental disorders, explaining cytoplasmic accumulation due to nuclear import defects.

This study identifies a novel pathway where MAP4K3 inhibits Sirtuin-1 to suppress LKB1-AMPK, thereby activating mTORC1 in response to amino acids.

This paper demonstrates the use of induced pluripotent stem cells to create an isogenic system for studying genetic influences on cell-cell interactions in type 1 diabetes.

The paper identifies ubiquitination of G3BP1 as a mechanism required for heat shock-induced stress granule disassembly through interaction with FAF2 and p97/VCP.

The paper shows that stress-induced ubiquitination is essential for recovery of cellular activities following heat stress.

This paper introduces a system for high fidelity reconstitution of stress granules and nucleoli in mammalian cellular lysate, bridging in vitro and live cell studies of membraneless organelles.

This study shows that MAGE-B2 enhances stress tolerance by reducing G3BP and suppressing stress granules, protecting male germline cells from heat stress.

This study shows that harmine enhances the efficacy of HIV-1 latency-reversing agents by increasing transcription factor availability and reducing HEXIM1 expression.