Nigel W. Bunnett

This study shows that EP4 receptor internalization and compartmentalized signaling in DRG nociceptors mediate PGE2-induced pain, suggesting new strategies for inflammatory pain management.

This paper reports the cryo-EM structure of a TrkA-neutralizing antibody complex, revealing its mechanism of isoform selectivity and therapeutic potential for chronic pain.

This study identifies synaptic vesicle endocytosis in nociceptors as a driver of chronic pain and shows that targeting it with CRISPR/dCas9-R via lipid nanoparticles provides long-lasting pain relief without affecting acute pain responses.

This paper introduces SynPARs, synthetic protease-activated receptors that enable cells to sense and respond to protease activity, demonstrating their use in counteracting hyperalgesia in mice.

This study shows that inducible PKA activation in osteoblasts leads to high bone turnover and disease-like phenotypes in mice.

This study shows that PAR2 endosomal signaling amplifies and sustains histamine-induced pain in IBS by maintaining H1R activity.

This study shows that targeting mGlu5 in endosomes improves analgesia by inhibiting nuclear ERK1/2 signaling and reducing neuronal excitability in pain models.

This study investigates the role of cathepsin S and X in inflammatory bowel diseases using activity-based probes and mouse models, finding that cathepsin S contributes to some symptoms but pharmacologic inhibition may have unintended effects.

This study shows that targeting protease-activated receptor 2 (PAR2) signaling in organelles using nanomedicines provides sustained analgesia in preclinical models of inflammatory bowel disease.

The paper identifies a druggable EP2 receptor in Schwann cells that encodes PG-mediated persistent inflammatory pain without affecting protective inflammation.

The paper designs TrkA agonists that activate neuronal differentiation and neurite outgrowth without triggering pain-related gene expression.

This study identifies a secreted protease from Bacteroides fragilis that cleaves PAR2, leading to intestinal inflammation and pain in mouse models.

This paper identifies NRP1 as a co-receptor for NGF and TrkA pain signaling and shows that targeting NRP1 or GIPC1 can reduce chronic pain without opioid use.