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Therefore, we reasoned that expression of CIITA mutants which fail to localize to the nucleus should not mediate increased Gag processing or enhanced infectious virus release.
This process is uncoupled in C. intestinalis Hox1 mutants, which fail to specify the ASPs.
The oskar mRNA localisation phenotype of slmb germline clones resembles that of par-1 mutants, which fail to repolarise the oocyte microtubule cytoskeleton (Shulman et al., 2000).
These gene ontologies are consistent with the phenotype of rx3 -/- mutants which fail to complete optic vesicle morphogenesis and exhibit expanded forebrains.
This is similar to corolla mutants, which fail to show a discernible SC structure when assayed by SIM (data not shown).
We next tested whether the synthetic sterility in the RNAi assays phenocopied that of fbf-1 fbf-2 double mutants, which fail to transition from spermatogenesis to oogenesis (Crittenden et al. 2002).
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As described above we have introduced the same point mutation in the human clathrin heavy chain as in one of the yeast TS-clathrin mutants, which failed to trimerize at the non-permissive conditions.
Overexpression of the PUM2 mutant which fails to interact with Aurora-A, and depletion of PUM2 result in a decrease in the amount of Aurora-A.
The G39A mutant, which failed to discriminate between specific and non-specific RNA binding, was also inactive in DNA demethylation as well as activation of EGFP expression.
Overexpression of the PUM2 mutant, which failed to interact with Aurora-A, and depletion of PUM2 both led to the destabilization of Aurora-A (Figure 3).
The CIITA L1035P mutant, which fails to translocate to the nucleus [58], demonstrated increased Gag processing and virus release compared to vector-only control, suggesting a cytoplasmic role for CIITA in the later stages of the HIV infection cycle.
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