IndraLab

Statements


USP1 activates MYC. 10 / 10
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eidos
"Taken together , these results indicate that USP1 promotes the expression of c-Myc by regulating KDM4A ."

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"We found that R1881 induced a significant increase in NKX3.1 (a positive control) transcript in RV1 cells, but it failed to induce the c-Myc transcript, and USP1 knockdown reduced the c-Myc or NKX3.1 transcript similarly, with or without R1881."

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"Conclusions: Our results suggested that high expression of USP1 promotes bladder cancer progression by stabilizing c-MYC; hence, USP1 may serve as a novel therapeutic target for treating bladder cancer."

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"Inhibition of USP1 in DLBCL cells led to decreased expression of MAX and MYC and subsequently suppressed the activation of MYC and its downstream targets."

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"We found that overexpression of USP1 increased the stability of MAX and MYC protein in 293T and RL-4RH cells treated with cycloheximide (CHX) (Fig. 4f, g)."

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"USP1 Upregulates the c-MYC Pathway."

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"The results showed that USP1 overexpression significantly increased the activity of some signaling pathways, especially c-MYC, ATF2/3/4, and SP1 (Figure 4C)."

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"Moreover, USP1 expression increased the c-MYC luciferase reporter activity in a dose-dependent manner (Figure 4D)."

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"Next, we performed a cycloheximide assay to determine whether c-MYC protein levels are regulated by USP1 over time, and we found that USP1 expression increased the half-life of c-MYC, whereas USP1 C90S failed to rescue the half-life of c-MYC (Figure 5G)."

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"In summary, our results showed that USP1 deficiency downregulated c-MYC, which promoted tumor growth in vivo."