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. Author manuscript; available in PMC: 2012 Aug 5.
Published in final edited form as: Mol Cell. 2011 Aug 5;43(3):381–391. doi: 10.1016/j.molcel.2011.05.033

Figure 6. XLMR patients-derived CUL4B mutants cannot rescue Cul4b knockdown phenotype.

Figure 6

(A) PC12 cells were transduced with retrovirus encoding wild type or mutants CUL4B along with retrovirus encoding shRNA targeting Cul4b, and transduced cells were selected by puromycin treatment. Neurite-extending cells were counted 4 days after NGF treatment (upper panel) or protein expression was determined by immunoblot analysis (lower panel). Error bars represent S.E. from three independent experiments. ** indicate p<0.01 by t test.

(B) HEK293T cells were transiently transfected with an expression vector for myc-tagged wild type or mutant CUL4B. The expression of ROC1, DDB1 and CSN5 (upper panel) and their binding with wild type or mutant CUL4B (lower panel) were determined by direct immunoblotting or IP-western analysis using indicated antibodies.

(C) HEK293T cells were transiently transfected with an expression vector for myc-tagged wild type or mutant CUL4B and treated with cycloheximide for indicated time. Cell lysates were subjected to immunoblot analysis (IB) with indicated antibodies. Band intensity was measured by NIH Image J (version 1.44k).

See also Figure S5.