Cheryl L. Stucky

This study uses automated behavioral recording to assess paclitaxel-induced neuropathy in mice, finding a consistent postural phenotype that is not fully reversed by gabapentin.

The paper shows Samd14 maintains autophagy balance in red blood cell precursors during acute anemia by interacting with PI3P and modulating VPS34 activity.

The paper shows clonazepam activates TRPM8 ion channels, which may explain its efficacy in treating burning mouth disorder.

This study shows that keratinocytes contribute to mechanical and cold hypersensitivity after traumatic nerve injury and that pannexin-1 activation is critical for this effect.

This study establishes a heat-induced pain model in Fabry disease and identifies a heat shock protein-TRPA1 regulatory axis as a key mechanism.

The paper identifies p11 release from Schwann cells as a driver of sensory neuron hyperexcitability in a genetic rat model of Fabry disease.

The paper shows that keratinocyte Piezo1 contributes to paclitaxel-induced mechanical hypersensitivity by sensitizing keratinocytes to mechanical stimulation.

The paper identifies gut microbiota and metabolites as drivers of chronic sickle cell disease pain by altering vagus nerve activity.

The paper uses SCD patient-derived iPSCs to study sensory neuron function and identifies plasma factors that sensitize neurons to pain stimuli.

This study identifies Piezo1 as the major mechanotransducer in keratinocytes for detecting mechanical stimuli and transmitting tactile information to sensory neurons.

This study shows TRPA1 inhibition enhances KOR activity in sensory neurons, leading to analgesia, and identifies TRP channel regulation of GPCR activity as a novel mechanism for peripherally mediated pain relief.

This study investigates sex-based differences in endogenous opioid engagement during contextual control of pain tolerance and expectation in mice.

The paper identifies Piezo2 expression in neuronal and non-neuronal cells of the rat peripheral sensory pathway and links its elevation to pain conditions.

This study identifies TRPC5 as a mediator of inflammatory mechanical pain using knockout mice and pharmacological inhibitors, showing its role in pain behaviors induced by lysophosphatidylcholine.

This study shows keratinocytes are essential for normal cold and heat sensation in mammals through calcium release and ATP-P2X4 signaling.