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In this study we found that the ΔF508/V510D mutant was active while we failed to detect activity when V510D was introduced into Cys-less CFTR (9).
Analysis of the activity of CDK9's S175A and S175D mutants showed that CDK9 S175A mutant was active and S175D - inactive.
Nevertheless, the fact that the mutant was active against AZO-CMC, suggest that the substitution G251D, at least in combination with V259D, have a different impact on substrate specificity.
The Cry4Ba-L152D mutant was active against A. aegypti while the mutants Cry4Ba-E159K and Cry11Aa-V142D were inactive (Table 1).
CDK9 S175A mutant was active and S175D – inactive, and dephosphorylation of CDK9's Ser175 upregulated HIV-1 transcription in PP1-dependent manner.
Neither mutant was active with either m-galactarate or d-galacturonate, confirming their importance.
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However, the finding that a p73-PxxP mutant is active in transcription activation but not in apoptosis, argues that transcription activation might be required, but not sufficient, in mediating apoptosis.57 Interestingly, a similar mechanism was proposed for p53.
Our data indicate that this C94R/C99R eNOS mutant is active.
This mutant is active and has an increased stability (ΔTm=3 °C, Δ ΔGu =1.73 kcal/mol) relative to the wild-type enzyme.
Overnight expression of a single copy of swe1K594R from a GAL promoter resulted in elongated buds, similarly to overexpression of wild-type Swe1 (Figure 1D), indicating that this mutant is active.
Interestingly, the single L266K mutant is active for ubiquitin chain formation but deficient in Miro1 ubiquitination.
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