Paz Duran

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 study identifies peripheral nociceptor hyperexcitability as a mechanism underlying pain in DM1 using a mouse model.

This study shows that transient myotonia can cause long-lasting pain by altering nociceptive processing and identifies NaV1.8 as a target for analgesics.

This study shows MrGPRX1 signals from endosomes to sensitize TRPV1, enhancing itch signaling, and identifies pathways involved in this process.

This study investigates the role of endocytic mediators in itch transmission, finding that disrupting AAK1 and Dnm1/Dnm3 reduces scratching behavior without affecting motor function or anxiety.

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

This study shows that CBD3063, a CRMP2 modulator, reduces OA pain in rodents by decreasing CaV2.2 membrane expression and neural activity.

The paper develops a CRMP2-Ubc9 inhibitor that reduces NaV1.7 activity and alleviates trigeminal neuropathic pain in rats.

The paper identifies a unique NaV1.7 domain that can be targeted to produce analgesia by disrupting its interaction with CRMP2.