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USP22 binds E2F6. 13 / 16
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"Therefore, we validated the interaction of E2F6 and USP22; the results revealed that E2F6, a pocket protein-independent transcription repressor, was capable of interacting with USP22 ( Fig. 1 C–E), in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Importantly, we found that the function of the USP22-E2F6 axis in promoting tumor cell growth was fulfilled by a decrease in DUSP1 activities, wherein E2F6 could directly bind to the promoter region o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Therefore, the USP22-E2F6 axis has a tumor-promoting capacity in HCC, with the function to downregulate DUSP1 activities."
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"Therefore, we validated the interaction of E2F6 and USP22; the results revealed that E2F6, a pocket protein-independent transcription repressor, was capable of interacting with USP22 ( Fig. 1 C–E), in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Thus, herein we provide the evidence that DUSP1 inhibition by the USP22-E2F6 axis is the upstream event that activates AKT signaling and drives HCC growth."
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"These results indicate a functional significance of the interaction between USP22 and E2F6 in HCC."
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"To explore the functional importance of USP22-E2F6 regulation in HCC, we examined the transcriptional profiles of Huh7 cells with or without USP22 or E2F6 silencing by RNA-seq."
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"These results indicate a functional significance of the interaction between USP22 and E2F6 in HCC."
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"Overall, these results suggest that USP22-E2F6 regulation is a clinically relevant event in HCC."
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"Moreover, it has been demonstrated that the deubiquitinating enzyme USP22 can directly interact with and stabilize E2F6 in HCC cells, which indicates the presence of corresponding E3 ubiquitin ligases of E2F6 forming a dynamic bidirectional regulatory system for ubiquitin modifications 47."
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"Therefore, our data indicate that repression of DUSP1 transcription may underlie the function of USP22-E2F6 in HCC."
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"In this study, we identified E2F6 as a novel target of USP22 and provided evidence that USP22-E2F6 regulation promoted AKT hyperactivation and tumor growth."
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"Furthermore, the USP22-E2F6 regulation was manifested by the correlation in the expression patterns of USP22 and E2F6 in human HCC tissues, underlining the clinical relevance of the deubiquitination e[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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