Single Protein Found to Modulate Multiple Sensory Experiences in Mice

Researchers at Tsinghua University identified CRELD1 as a key protein influencing how mice perceive touch, temperature extremes, pain, and itch. Removing this protein significantly reduced responses across all these sensory modalities. The protein appears to regulate sodium channels essential for nerve signal transmission, suggesting broad therapeutic potential.

Researchers at Tsinghua University, led by Bailong Xiao, discovered that the protein CRELD1 plays a central role in modulating multiple sensory experiences in mice, including touch, temperature extremes (heat and cold), pain, and itch. In experiments published in Nature Neuroscience in 2026, mice with the Creld1 gene disrupted showed significantly reduced responses across all these modalities—withdrawal from light touch, delayed reactions to thermal stimuli, diminished pain sensitivity, and less scratching after histamine injection. The effect was specific to sensory neurons: when CRELD1 was deleted only in dorsal root ganglion neurons near the spinal cord, similar deficits emerged, ruling out general motor or cognitive impairments. Despite intact initial stimulus detection, these neurons failed to generate strong electrical signals due to weakened sodium channel activity—CRELD1 was found to bind and enhance several sodium channels, particularly Nav1.7, crucial for nerve impulse propagation. Increasing CRELD1 boosted sensitivity, while its absence reduced neuronal firing thresholds and signal strength. This suggests CRELD1 acts as a broad modulator of sensory signaling rather than a direct detector of stimuli. The study’s findings stem from a CRISPR-based screening approach targeting 20 candidate genes in newborn mice, with Creld1 emerging as uniquely impactful. However, human relevance remains uncertain: two human variants of CRELD1 were tested, and only one enhanced sodium