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Our finding that CBP stabilizes WRN through acetylation has been further examined by expressing WRN acetylation mutant in cells.

The analysis by Native-PAGE also showed that most forms of the C9/20/53/63/91A mutant in cells are monomer, but not dimer.

The heterotypic complementation obtained for SINV ΔDLP mutant in cells expressing E3 revealed a notable case of functional analogy that reinforced the importance of anti-PKR mechanisms for virus replication in vertebrates.

We expressed the dominant-negative dynamin-K44A mutant in cells treated with EHD2 siRNA.

Conversely, we asked whether expression of a Beclin 1 S90E phosphomimetic mutant in cells lacking detectable endogenous Beclin 1 could bypass the inhibitory effects of dominant negative MK2.

When we expressed the mutant in cells, we found that it exhibited a diffuse cytoplasmic localization and did not concentrate on the cortex.

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This pattern of lengths of cell cycles was not observed in embryos mutant in cell cycle factors.

Secondly, aggregation associated with the expression of the P182L-HSPB1 mutant in cell models was significantly reduced by the overexpression of wild-type HSPB8 (Carra et al., 2010).

We tested these mutants in cells with time-resolved fluorescence resonance energy transfer and death assays, and show remarkable agreement with the calculations.

This could account for the more pronounced effects of these mutants in cells bearing longer neurites (>50 µm) [10].

Since some misfolded tyrosinase mutants may fold and recover their enzymatic activity below 37°C [24] we have expressed the mutants in cells cultivated at 31°C.

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