IndraLab

Statements


USP15 activates TBX3. 5 / 5
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"Consequently, USP15 deficiency inhibits melanoma tumor cell proliferation and xenografted tumor growth in the TBX3-dependent manner, which is consistent with reported USP15 function in melanoma development (Fig. 5h, Supplementary Fig. 4d, e)."

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"This stabilization of TBX3 depends on USP15’s DUB activity, since wild-type USP15, but not the USP15 mutant, restored TBX3 loss caused by USP15 depletion (Fig. 1g, h), and ectopic USP15 lost the function to prolong TBX3 half-life (Fig. 1i, Supplementary Fig. 1e, f)."

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"To further evaluate the clinical significance of USP15 mediated TBX3 homeostasis and understand their correlation in tumorigenesis, we performed immuno-histochemical (IHC) staining to examine the expression of these factors in patient samples."

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"Therefore, we asked whether USP15-mediated TBX3 stabilization could be a molecular signature-related event."

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"Activated BRAF/MAPK pathway functions partially through USP15-mediated TBX3 stabilization, thus genetic knockout of Usp15 leads to disrupted organ development and tumorigenesis comparable to Tbx3 mutants."