IndraLab

Statements

USP13 binds MAP2K3. 7 / 7
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"Our understanding of the USP13-MKK3 axis in this study primarily focuses on CRC, while its role in other cancers remains insufficiently explored."
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"Meanwhile, blocking ubiquitination at the K32 site of MKK3 (K32R mutation) mimics the USP13 overexpression phenotype, further confirming that this site is the core target of the USP13-MKK3 regulatory axis."
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"Additionally, whether the USP13-MKK3 axis can be effectively combined with existing targeted therapies (such as MEK, PI3K, and BRAF inhibitors) or immunotherapies (such as PD-1/PD-L1 antibodies) to enhance therapeutic efficacy requires further clinical trial data."
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"USP13 interact with MKK3."
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"Specifically, USP13 directly interacts with the C-terminal domain of MKK3 through its UBA domain and, relying on its deubiquitinase activity, selectively removes K48-linked ubiquitination (especially at the K32 site) on MKK3, thereby inhibiting its degradation via the proteasome."
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"Finally, we demonstrated that p38 activation is both sufficient and necessary for the tumor-promoting effects downstream of the USP13-MKK3 axis."
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"Therefore, further investigation is needed to elucidate the specific roles and mechanisms of the USP13-MKK3 axis in different cancers."
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