Quantitative FRET UPR induction assay is used to measure IRE1 and BIP association and dissociation by a variety of ER misfolded proteins and by an important BiP substrate-binding domain mutant, significantly enhancing the evidence for the allosteric UPR induction model.

A genetic screening approach identifies RNA binding proteins that enhance or inhibit the accumulation of CD138+ plasma cells in vitro, and chimeric mouse models demonstrate that YTHDF2 promotes the accumulation of antibody secreting cells in vivo.

A method has been developed to characterize the expressed biochemical activities of gut microbial communities using retrievable, microscopic, fluorescent-labeled glass beads containing chemically bound surface biomolecules.

The immunoglobulin superfamily cell surface protein Sticks and Stones is a binding partner for the Lar Drosophila receptor tyrosine phosphatase that mediates Lar's developmental functions at the larval neuromuscular junction, mushroom body, and adult optic lobe.

Genetic and protein analyses in vitro and in vivo identifies Id4 as a novel regulator of stem cell quiescence in the adult hippocampus.

Laboratory-based methods are presented that produce filamentous tau aggregates with the same structures as those observed in neurodegenerative disease.

Comprehensive proteomic investigation and functional studies unravel an essential role of differentiated glioma cell-secreted fibromodulin (FMOD) in regulating glioblastoma tumor growth by inducing angiogenesis by activating integrin-dependent Notch signaling in endothelial cells, highlighting FMOD as a potential therapeutic target.

Centriole integrity is ensured by the connection between the inner scaffold and microtubule triplets through POC16/WDR90 proteins.

Cytological analyses combined with in vitro liposome reconstitution reveal that yeast SUN domain protein, Mps3, shows meiosis-specific phosphorylation in the luminal region of the nuclear envelope during meiosis for chromosome motion and nuclear envelope remodelling.

A new native prion protein aggregation assay shows that syntaxin-6, a risk factor for sporadic Creutzfeldt–Jakob disease, delays prion protein fibril formation and prolongs the presence of toxic aggregation intermediates.