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(D) CHO cells transfected with indicated PML-RARA mutants were treated with 10 µmol/L AS2O3 for 2 h.

(C) 293T cells harboring the expression plasmids of PML-RARA mutants were treated with or without 2 µmol/L AS2O3 for 4 h.

Furthermore, when FL-VASP mutants were treated with BAY60, only the FL-VASP/239D group showed reduced migration compared to its VEH controls.

MPK6 activation was totally compromised when mkk3 mutants were treated with Salmonella, revealing that Salmonella-induced activation is mediated by MKK3 (Fig. 6a).

Cells transiently expressing these phospho-deficient mutants were treated with Adr, UV or γ-IR and differences in phosphorylation at the remaining unsubstituted phosphorylation sites were evaluated (Figure 4B).

There was no improvement of fat-6;fat-7 growth rate or fat stores when these mutants were treated with RNAi corresponding to the additional acyl-CoA oxidases, either of the bifunctional enzymes, or dhs-28.

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All these genes, (plus three which marginally fail the significance test for mutB but are significant when all the 3A mutants are treated as a single group) are summarised in Table 1.

To assess whether EGF mediated AKT activation is dependent upon Tyr176-phosphorylation, MEF1&2KO cells expressing AKT or Y176F mutant were treated with EGF ligand.

Recombinant proteins of wild Nm23-H1 and C109A mutant were treated with 2.5 mM oxidized glutathione (GSSG) or 5 mM reduced glutathione (GSH) for 1 h at 37°C.

When cells expressing this mutant were treated with LMB, the 32 kDa band still appeared.

All RNA samples of the wild-type strain and D hfq mutant were treated similarly throughout the experimental steps.

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