Dongzhi Ran

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

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.