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. 2011 Mar 21;192(6):993–1004. doi: 10.1083/jcb.201011111

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Figure 7. — mCK1ε/δCT(278–364) rescued Wnt-3a–dependent neurite outgrowth otherwise inhibited by CK1δ siRNA. (A) Wnt-3a–dependent neurite outgrowth in TC-32 cells treated with hCK1δ siRNA targeting 3′-UTR sequence and transiently transfected with empty vector (pcDNA3.3 Ctl.) or construct expressing mouse full-length CK1δ, full-length CK1ε, or chimera consisting of CK1ε N-terminal and kinase domains plus residues 278–364 from mouse CK1δ C-terminal domain. The presence of neurites was quantified in ∼30 cells expressing Myc-tagged CK1 protein for each treatment group. Data are from one of two experiments with similar results. (B) Immunoblot analysis of ectopically expressed Myc-tagged CK1 proteins, endogenous CK1δ, and HSP70 in the neurite outgrowth experiment. Results illustrate the efficacy and specificity of knockdown with siRNA directed against human CK1δ 3′-UTR sequence.