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At is conjugated to the K720 residue of Cul-1 (and to an homologous lysine in all other Cullins as well) using Uba3 (E1), Ubc12 (E2), and Roc1 (E3) [28,29,30,31]. This modification is in turn cleaved off by the multisubunit COP9 Signalosome (CSN) [32,33]. Since mutations in the pathways that conjugate and remove Nedd8 are detrimental, the current model is that cycles of neddylation and de-neddylat
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Nally substitute for Roc2. We tested this by introducing a Roc1a transgene into the Roc2KG mutant background. Even in this genotype, Roc1a bound to Cul1 but not detectably to Cul5 (Fig. 8). Moreover, as we show in Fig. 6G, the pool of Cul5 available for binding Roc1a is greatly reduced in Roc2 mutant animals relative to wild type. Thus, the Cul1 and Cul5 E3 ligase complexes form independently of o
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