IndraLab

Statements

USP29 binds CDK1. 9 / 9
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"In conclusion, our study identifies the previously unknown oncogenic role of CDK1‐USP29 axis in regulating the stability of TWIST1 and demonstrates their clinical relevance as therapeutic targets in TNBC."
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"In addition, purified GST‐USP29 but not GST could interact with His‐CDK1 in vitro, indicating the direct interaction between USP29 and CDK1 (Figure  xref )."
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"CDK1 Binds and Phosphorylates USP29."
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"In this study, we reveal several unexpected tumor‐promoting functions and the clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide preclinical evidence demonstrating that targeting CDK1‐USP29 axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC (Figure  xref )."
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"Together, these results uncover a previously unrecognized function of USP29 in tumor progression of TNBC through stabilizing TWIST1.2.4 CDK1 Binds and Phosphorylates USP29."
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"Collectively, these results suggest that CDK1 directly interacts with and phosphorylates USP29 other than TWIST1.2.5 CDK1 Regulates TWIST1 Protein Stability, CSC Self-Renewal, and Cellular Sensitivity to Chemotherapy."
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"In addition, purified GST‐USP29 but not GST could interact with His‐CDK1 in vitro, indicating the direct interaction between USP29 and CDK1 (Figure 4D)."
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"Importantly, we provide preclinical evidence demonstrating that targeting CDK1‐USP29 axis might be effective to destabilize TWIST1 which decreases the CSCs population, tumor metastasis, and chemo‐resistance of TNBC."
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"Taken together, the findings reveal a previously unrecognized tumor‐promoting function and clinical significance of the CDK1‐USP29 axis through stabilizing TWIST1 and provide the preclinical evidence that targeting this axis is an appealing therapeutic strategy to conquer chemo‐resistance and metastasis in TNBC."
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