IndraLab

Statements

BMAL1 binds USP4. 4 / 4
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"Functional rescue experiments confirmed the critical role of the USP4–ARNTL axis in conferring protection."
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"This approach revealed ARNTL, a core circadian clock component xref and a known repressor of ferroptosis, as a potential binding partner. xref Subsequent co‐IP assays in HUVECs confirmed a robust endogenous interaction between USP4 and ARNTL, which was reciprocally validated (Figure  xref )."
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"These findings identify SR‐induced clock rhythmic ferroptosis as a critical pathological driver of flap failure and propose a novel exosome‐based strategy targeting the USP4–ARNTL axis to enhance skin barrier integrity and flap survival, offering translational potential for clinical reconstructive surgery."
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"Additionally, this USP4–ARNTL axis was substantiated by their correlated high expression in viable human flap tissues showing minimal ferroptosis and confirmed through rescue experiments where USP4 mediated clock rhythmic ferroptosis regulation via ARNTL."
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