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• W4293485808 abstract "Cop9 signalosome (CSN) regulates the function of cullin-RING E3 ubiquitin ligases (CRLs) by deconjugating the ubiquitin-like protein NEDD8 from the cullin subunit. To understand the physiological impact of CSN function on the CRL network and cell proliferation, we combined quantitative mass spectrometry and genome-wide CRISPR interference (CRISPRi) and CRISPR activation (CRISPRa) screens to identify factors that modulate cell viability upon inhibition of CSN by the small molecule CSN5i-3. CRL components and regulators strongly modulated the antiproliferative effects of CSN5i-3, and in addition we found two pathways involved in genome integrity, SCFFBXO5-APC/C-GMNN and CUL4DTL-SETD8, that contribute substantially to the toxicity of CSN inhibition. Our data highlight the importance of CSN-mediated NEDD8 deconjugation and adaptive exchange of CRL substrate receptors in sustaining CRL function and suggest approaches for leveraging CSN inhibition for the treatment of cancer." @default.
• W4293485808 created "2022-08-29" @default.
• W4293485808 creator A5005417134 @default.
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• W4293485808 date "2022-08-29" @default.
• W4293485808 modified "2023-10-16" @default.
• W4293485808 title "Adaptive exchange sustains cullin–RING ubiquitin ligase networks and proper licensing of DNA replication" @default.
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• W4293485808 doi "https://doi.org/10.1073/pnas.2205608119" @default.
• W4293485808 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36037385" @default.
• W4293485808 hasPublicationYear "2022" @default.
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