A single protein that helps drive responses to touch, temperature, pain and itch could offer a new drug target
· Medical Xpressby Andrew Zinin, Medical Xpress
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A light brush, a hot surface and an irritating itch all activate different sensory pathways, yet researchers have determined that, in mice, these otherwise distinct responses share a molecular helper. A team led by Bailong Xiao at Tsinghua University found that removing the protein CRELD1 weakened the animals' reactions to touch, heat, cold, painful pressure and itch. But how can one protein influence so many different sensations?
The team's article, published in Nature Neuroscience, shows that CRELD1 is a broad regulator of sensory responses, supporting sodium-channel activity that helps neurons generate the electrical impulses that carry information onward after a stimulus has been detected.
A gene that stood out
To identify the genes involved in sensation, the researchers used CRISPR to disable selected genes in newborn mice, then tested the animals as they grew. After validating their method against genes with established sensory roles, the team screened 20 candidates. One, Creld1, stood out for the breadth of its effects.
Mice with the disrupted gene withdrew their paws less often when touched with fine filaments or a soft brush. They also responded less strongly to painful mechanical stimulation and took longer to react to hot and cold surfaces.
To make sure these changes came from sensory neurons, the researchers used a second genetic method to delete Creld1 specifically in neurons clustered beside the spinal cord. The mice showed similar deficits. They also barely scratched after injections of histamine, an itch-triggering chemical, and scratched less in response to other itch-inducing substances.
The body weight, movement and coordination of the mice all remained normal in the tests. A general inability to move therefore could not readily explain their muted reactions.
The next step was to find where the sensory process was faltering.
Detecting a stimulus is only the start
The machinery that initially detects touch, temperature and irritating chemicals appeared to be working. Sensory neurons lacking the CRELD1 protein still showed responses comparable to those of unmodified neurons when exposed to those stimuli.
But detecting something and sending a strong electrical signal are separate jobs.
To generate electrical impulses, neurons rely on sodium channels—proteins that allow electrically charged sodium ions to cross the cell membrane. The researchers found that the CRELD1 protein binds to several of these channels and boosts their activity.
Without CRELD1, sodium currents weakened. The neurons needed stronger stimulation to fire and they produced fewer electrical impulses. Increasing CRELD1 production did the opposite: It strengthened sodium currents and made mice more responsive to touch, heat and cold.
Together, the experiments explain how CRELD1 can influence several senses without being the specific receptor that detects a particular stimulus.
The authors suggest that the contact point between CRELD1 and sodium channels "might offer a precision target for drug development." However, the mouse results do not establish a treatment, and the human protein presents a complication.
Two human versions of the protein were tested in cultured cells, but one boosted a sodium channel's activity while the other did not. Researchers still need to determine which versions predominate in human sensory neurons.
Any attempt to use this discovery in the development of a treatment against pain or itch would therefore need to establish how the mechanism works in people—and whether unwanted sensations can be reduced without dulling the everyday signals that help protect the body.
Written for you by our author Andrew Zinin, edited by Lisa Lock, and fact-checked and reviewed by Robert Egan—this article is the result of careful human work. We rely on readers like you to keep independent science journalism alive. If this reporting matters to you, please consider a donation (especially monthly). You'll get an ad-free account as a thank-you.
Publication details
Yan Jiang et al., Behavioral genomics identifies Creld1 as a cross-modal regulator of somatosensation, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02484-w
Journal information: Nature Neuroscience
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Andrew Zinin
Master's in physics with research experience. Long-time science news enthusiast. Plays key role in Science X's editorial success. Full profile →
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