Sunlight is essential for human health, yet its damaging effects on skin cells continue to reveal new layers of complexity.
In research published in Nature Communications, scientists at the University of Chicago describe how ultraviolet radiation interferes with a crucial protein called YTHDF2.
It is an unexpected finding that may help explain why some sunburns contribute to long-term disease.
According to a statement from the University of Chicago Medical Center, the team observed that levels of YTHDF2 dropped sharply when skin cells were exposed to UV.
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The protein normally helps moderate immune activity by managing the turnover of specific RNA molecules.
Without it, the researchers say, the cells respond to UV damage with far more intense inflammation.
Small RNA signals with big consequences
The study focused in particular on a short RNA known as U6. Under normal conditions, U6 is broken down as part of routine cell maintenance.
Under UV stress, however, the molecule accumulates and migrates into endosomes which are cell compartments where it typically does not appear.
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Inside these structures, U6 can activate a receptor called TLR3, which is known for driving strong inflammatory responses.
The team also identified a transport protein that shuttles U6 into the endosome and noted that YTHDF2 normally accompanies it.
When the protective protein is missing, U6 is able to trigger TLR3 freely, amplifying inflammation.
Implications for prevention and treatment
The findings outline a previously unrecognized surveillance mechanism that keeps inflammation in check after sun exposure.
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By mapping how RNA and proteins interact during UV stress, the researchers suggest that future therapies might aim not only to shield the skin from UV rays but also to interrupt harmful signaling cascades that follow.
The study opens the door to new strategies for preventing UV-related skin cancer by stabilizing or mimicking this regulatory pathway.
Sources: Science Daily, and Nature Communications.
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