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USP15 activates TGF-β/Smad. 2 / 2
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"In addition, there is a fundamental difference in wound healing between mice and humans, as contraction is the primary mechanism for murine skin repair, 33 and further studies could explore the clinic[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"We hypothesized that USP15 deubiquitinated TGF-β receptor I to enhances TGF-β/Smad signaling, which in turn up-regulated USP15, leading to enhancement of the proliferation, migration, invasion, and collagen deposition of hypertrophic scar–derived fibroblasts in vitro."
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