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. 2009 Sep 23;284(49):33789–33794. doi: 10.1074/jbc.M109.048983

FIGURE 5.

FIGURE 5.

Phosphorylation of MyoCD by ERK1/2 reduces its induction of SM gene transcription. A and B, 10T1/2 cells were transfected with cDNAs for the full-length MyoCD or its quadruple phosphodeficient alanine (4×A) or phosphomimetic aspartate (4×D) mutant, along with firefly luciferase reporters for SM α-actin (A) or SM22 (B) promoters and Renilla luciferase driven by thymidine kinase promoter control reporter. Following 24 h of transfection, the luciferase activity was measured as described under “Experimental Procedures.” C and D, 10T1/2 cells were transfected with cDNAs for the full-length MyoCD or its quadruple 4×A or 4×D mutant for 24 h, and cells were analyzed for mRNA levels of SM α-actin (C) and SM22 (D) by quantitative real time PCR. E and F, HT-1080 cells were transfected with cDNAs for the full-length MyoCD or its quadruple 4×A or 4×D mutant for 24 h, and cells were analyzed for protein expression of SM α-actin (E) and SM22 (F) by Western blotting with corresponding antibodies. Data represent mean ± S.D. from a representative (of three) experiment performed in triplicate (*, p < 0.05).