A key cellular stress granule protein, G3BP1, is critical for efficient norovirus infection, representing the first pan-norovirus, pro-viral factor identified to date.

OptoGranules reveal the function of G3BP1 as a stress granule scaffold and demonstrate that protracted stress granule assembly is sufficient to drive neurodegeneration and the evolution of ALS-FTD pathology.

Two phosphorylation sites on 53BP1 are found to mediate interaction with TOPBP1-RAD9 and shown to be essential for assembling the G1 DNA damage checkpoint response apparatus.

53BP1 and BRCA1 antagonistically control a temporal choice of two distinct pathways to restart stalled replication forks in a DNA double stand repair-independent manner.

A single-cell assay reveals that the genetic rewiring that underlies PARP inhibitor resistance drives altered DNA double-strand break end resection pathway choice.

The RIF1-long and short splice variants show distinct ability to protect cells from replication stress by promoting 53BP1 nuclear bodies, representing the first described functional difference between the two variants.

Tumor Protein p53 Binding Protein 1 and Ubiquitin Specific Peptidase 28 engage p53 to promote mitotic efficiency.

The formation of long-term memory in mice requires an element of RNA granules that localizes messenger RNAs to dendrites.

Two homologous kinesin motors, KIF5A and KIF5B, have distinct functions in dendritic spine morphogenesis, and KIF5B plays a role in synaptic plasticity and memory.

Tim-3 promotes the ubiquitination and degradation of NF90, a novel virus sensor, and negatively regulates the NF90-SG pathway-mediated antiviral innate immunity.