IndraLab

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USP5 increases the amount of CCND1. 10 / 10
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"Our data showed that knockdown of USP5 decreased the level of CCND1 but not that of CCND2 or CCND3 in NSCLC cells (Figure 3C), which suggested that USP5-mediated deubiquitylation and stabilization of D-type cyclins is specific to CCND1."
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"Previous studies have shown that USP5 increases the expression of CCND1 in pancreatic cancer (22) and NSCLC (23)."
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"Nonetheless, our data showed that genetic manipulation of USP5 alone could modulate the CCND1 protein level in NSCLC cells in which USP22 was highly expressed, indicating that two members of the USP family, USP5 and USP22, can exert an additional effect in the stabilization of CCND1 via similar or distinct mechanisms."
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"In line with the above finding that genetic inhibition of USP5 suppressed the level of CCND1 protein, chemical inhibition of USP5 activity using WP1130 and G9 also produced a similar effect of downregulating the protein level of CCND1 in NSCLC cells (Figure 4C)."
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"A previous report (22) on short hairpin RNA (shRNA) barcode library screening showed that USP5 can upregulate the level of CCND1 protein in pancreatic cancer cells."
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"Recent studies have demonstrated that CCND1 can be upregulated by USP5, another member of the USP family, in pancreatic cancer (22) and NSCLC (23); however, the mechanism of action is still unclear.Given its deubiquitinating effect on multiple oncoproteins (24), the present study was performed to investigate whether USP5 upregulates the expression level of CCND1 protein in NSCLC via deubiquitination and stabilization of CCND1."
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"Further, our gain- and loss-of-function experiments demonstrated that overexpression of USP5 prevented endogenous CCND1 from polyubiquitinating in NSCLC cells and increased the CCND1 protein level (Figure 2E), whereas knockdown of USP5 produced the opposite effect (Figure 2F)."
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"Interestingly, USP5 overexpression remarkably increased the levels of CCND1 protein in NSCLC cells (Figure 1E), whereas knockdown of USP5 using its specific siRNA reduced the protein levels of CCND1 (Figure 1F)."
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"Overexpression of USP5 could significantly extend the half-life of CyclinD1, while knockdown of USP5 decreased the protein level of CyclinD1, which could be restored by proteasome inhibitor MG-132."
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"We found that USP5 increased the protein level of CCND1 in a concentration-dependent (Figure 1A) and time-dependent (Figure 1B) manner."
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