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Dominant-negative mutation of JNK (DN-JNK) is a mutant at these sites (on Thr and Tyr), which effectively suppresses paclitaxel-induced cell apoptosis in cancer cells [ 10].
However, the observation that rab7 T22N exhibits some rescue of the null mutant further indicates that it retains some wild-type function and does not obviously act as a genetically dominant negative mutant at these levels of overexpression in Drosophila.
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We also assayed phosphorylation states of the thylakoid proteins in the stn7 and stn8 mutants at these time points representative for night and day (Figure 3B).
To evaluate this hypothesis, structures of reciprocal single-site mutants at these 15 positions around the active site of BSP165 and TF MAN in complex with mannotriose were constructed and pKa calculations were carried out (Table 4).
However, we noticed that the general phenotypic features observed with rpl35 knockdown were common among the RP gene mutants at these later stages of embryonic development (2 4 dpf), when morphogenesis of primary organs systems is complete.
To explore the influence of the conserved charged residues on phospholipid transfer by PRELI-like domains, we decided to test mutants at these positions for function.
This was also the case for Phe37, Ala68, Gly292, Asn293, Phe373, and Tyr374 (some or all of the mutants at these positions had lower percent conversion values, but all those retaining activity showed essentially unchanged S stereoselectivity for 1– 3).
To test if the targeted residues affect formation of the E S complex, we determined the change in salt dependence for SRL cleavage by mutants at these positions [Δ n = nWt − nMut (Table 1 and Figure 1)].
These cell lines were either wild-type or mutant at the tumor suppressor gene, p53 (Table 1).
AVR-PikE was included in these experiments as it represents a naturally occurring point mutant at the important position 46 (His46Asn).
(B) Decreased Pri2 protein levels in the tah18-5I5 mutatthet the restrictive temperature.
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