IndraLab

Statements


RELA activates COPS5. 9 / 9
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"RelA-based NF-ĸB dimers were shown to upregulate the deubiquitinating enzyme CSN5."

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"In addition, p65 stimulated CSN5 activation, whereas a dominant negative IkappaBalpha mutant (IkappaBalpha 2SA) abolished p65 induced COPS5 promoter activation (XREF_FIG)."

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"Transcriptional Activation of CSN5 by p65 Is Required for TNF-alpha-Mediated PD-L1 Stabilization."

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"We demonstrated that COP9 signalosome 5 (CSN5), induced by NF-kappaB p65, is required for TNF-alpha-mediated PD-L1 stabilization in cancer cells."

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"Conversely, COP9 signalosome 5 (CSN5), induced by nuclear factor kappaB p65, is required for tumor necrosis factor-alpha (TNF-alpha)-mediated PD-L1 stabilization in cancer cells either by direct deubiquitination or by inhibiting ubiquitination and degradation of PD-L1 (XREF_FIG)."
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"P65, but not its heterodimeric partner p50, stimulated CSN5 activation through the p65 binding site, and mutation of the binding site on the COPS5 promoter abrogated p65 mediated COPS5 promoter activity (XREF_FIG)."

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"The NFκB pathway component p65 induces the CSN5 (COP9 signalosome 5), which is capable of inhibiting PD-L1 ubiquitination and therefore prolonging protein presence [63]."

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"Transcriptional Activation of CSN5 by p65 Is Required for TNF-α-Mediated PD-L1 Stabilization."

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"Transcriptional Activation of CSN5 by p65 Is Required for TNF-α-Mediated PD-L1 Stabilization."