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. 2013 Sep 9;288(43):31339–31349. doi: 10.1074/jbc.M113.484816

FIGURE 9.

FIGURE 9.

NUB1L or P97 suppresses the neddylation of CUL1. A, effect of NEDD8 and its mutants on the neddylation of CUL1. Transfection and Western blotting analysis were similar to that described in Fig. 1, A and B. Data were quantitated and presented as the means ± S.E. (n = 3). *, p < 0.05; **, p < 0.01; N.S., no significance. B, effect of NUB1L or P97 on the neddylation of CUL1. C, effect of knockdown of NUB1L or P97 on the neddylation of CUL1. The experimental condition is the same as in Fig. 1, C and D. E, schematic representation showing that NUB1L regulates proteasomal degradation of NEDD8 via the P97UFD1/NPL4 complex. The P97UFD1/NPL4 complex can recruit NEDD8 via NPL4 binding, whereas NUB1L forms a quaternary complex with P97UFD1/NPL4 by interacting with P97. In the complex the ATP hydrolysis by P97 triggers transfer of NEDD8 from NPL4 to NUB1L, by which NEDD8 is delivered to the proteasome for degradation.