Kimberly Gómez

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

This study identifies NaV1.7-dependent peripheral sensitization as a mechanism of chronic pain in Parkinson's disease and highlights CRMP2 regulation of NaV1.7 as a therapeutic target.

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 paper introduces a method to preserve human dorsal root ganglion neurons using Hibernate media, enabling easier access and transport for research.

This study investigates how anti-CV2/CRMP5 autoantibodies cause pain in paraneoplastic neurological syndromes and identifies potential treatments.

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.

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.

This study shows that SARS-CoV-2 Spike protein blocks VEGF-A/NRP-1 signaling, reducing pain and potentially contributing to asymptomatic transmission.

This study shows that non-SUMOylated CRMP2 forms an endocytic complex to internalize NaV1.7 channels, and inhibiting this complex restores sodium currents in mice with neuropathic pain.

This study shows that preventing CRMP2 SUMOylation reduces mechanical allodynia in female neuropathic pain models but not in males or other pain types.