IndraLab

Statements


COPS5 is produced. 9 / 9
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"Since JAB1 knockdown significantly decreased nuclear JAB1 expression, but not clearly decrease cytoplasmic JAB1 expression, the decrease in nuclear JAB1 expression may cause the decrease in nuclear β-[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Herin, METTL3 overexpression could increase the m 6 A methylation levels of COPS5, stabilizing COPS5 mRNA and upregulating COPS5 expression."

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"Introduction of DN-Jab1 into proliferating fibroblasts increased the level of p27 protein, thereby inducing growth arrest of the cells."

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"The mechanisms involved implies that CCL5 promotes the formation of the kappa-B p65/STAT3 complex, which activates COP9 signalosome 5 (CSN5) transcription, and then CSN5 further regulates the deubiquitination and stability of PD-L1, further inhibiting CD8+ T cell responses and thus leading to immune escape (67)( Figure 1 )."

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"Similarly, SENP1 increases androgen sensitivity to promote prostate cancer growth (31) and enhances invasion and metastasis activities of triple-negative breast cancer through elevating CSN5 transcription mediated by GATA1 deSUMOylation (15)."

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"SENP1 promotes triple-negative breast cancer invasion and metastasis via enhancing CSN5 transcription mediated by GATA1 deSUMOylation."

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"6 , 9 In this study, our data provide evidence that menin promotes the ubiquitination and degradation of PD‐L1 by inhibiting the expression of the deubiquitinating enzyme CSN5, thereby decreasing the stability of PD‐L1 in cells.CTLA4 and PD‐L1/PD‐1 are usually activated in TME and repress T cell‐mediated cytotoxicity."

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"Our studies implicate that Jab1 is required to remove post-translationally modified p53 and provide a novel target for p53-related cancer therapies."

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"We found that Jab1 (Jun activation domain-binding protein 1), a co-activator of AP-1, specifically interacted with Fank1."