J. C. Paton

This study shows that enhancing ER proteostasis with BIX rescues the function of epilepsy-linked NMDAR variants by improving their folding and trafficking.

This study identifies how inflammatory cytokines alter the proinsulin interactome in human islets, revealing new interactions and mechanisms involved in diabetes-related proinsulin dysregulation.

This study shows that the SpnIII phasevarion in S. pneumoniae affects multiple virulence traits and vaccine candidate expression, highlighting its importance in vaccine design.

This study investigates how Acinetobacter baumannii balances fatty acid synthesis and acquisition in different host niches during infection.

This study measures Neu5Gc serum biomarker levels in breast cancer patients and finds elevated levels at all disease stages, with high sensitivity and specificity for detection.

This study identifies CzcE and the CzcCBA efflux system as key factors in A. baumannii's resistance to cadmium stress and reveals metal ion homeostasis changes under cadmium exposure.

The paper identifies a novel Ca2+ signalling system in ER stress initiated by Ca2+ microdomains in human astrocytes and IP3R-deficient cells.

The paper shows dendritic cells have high eIF2 phosphorylation due to PERK activation, but this does not lead to chronic ISR or translation arrest, allowing them to adapt to stress.

The paper maps interactions of ER ubiquitin ligases and identifies a complex involving RNF26 that modulates innate immune signaling via the cGAS-STING pathway.

This study identifies the interdomain helix between IRE1α kinase and RNase domains as critical for transmitting conformational changes during ER stress, revealing its role in regulating oligomerization, RNase activity, and kinase function.

This study uses dual RNA-seq to show how a single SNP in Streptococcus pneumoniae affects bacterial and host gene expression, leading to differential tissue tropism and disease outcomes.

This study shows IRE1β suppresses IRE1α signaling during ER stress by blocking its activation and disrupting a feedback loop that regulates IRE1 expression.