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The SENP3 C532A mutant that lost de-SUMOylating activity did not change the Ub conjugation of Sp1 (Fig. 4A).
If the CAMP functions through a similar mechanism as the divalent cation in inducing the conformational changes of PhoQ, why the PhoQW104C-A128C muthat that lost the response to divalent cation limitation can still respond to the CAMP.
If the CAMP functions through a similar mechanism as the divalent cation in inducing the conformational changes of PhoQ, why the PhoQ W104C-A128C muthat that lost the response to divalent cation limitation can still respond to the CAMP.
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The effects were dependent on E2-CD81 interaction on the cell surface, since CD81-silenced Raji cells did not respond to both treatments; and an E2 mutant that lose the CD81 binding activity, could not trigger the responses of both Raji cells and PHB cells.
Although biological dependence upon pH has not been demonstrated thus far, it is plausible that the p.R337H mutant protein operates as a conditional mutant that loses its function only in cells undergoing a small increase in intracellular pH.
Norrin mutants that lose binding to Fz4CRD also fail to induce the luciferase reporter activity, in agreement with the SPR results and prior genetic data (Xu et al., 2004; Smallwood et al., 2007).
The clones that maintained detectable PCR products up to Tc or over were assumed as desired mutants and those that lost detectable products, the parental molecules.
Mutant strains that lose intracellular survival cannot carry out infection of their host; therefore, the virulence of Brucella depends upon its ability to survive and replicate within host cells.
In addition, an Srs2 mutant that has lost its ability to interact with the Rad51 protein is unable to disrupt the Rad51 nucleoprotein filament [26,27].
This finding suggests that HAdV-14p1 could be an immune escape mutant that has lost a potential neutralizing epitope, has modified postinternalization steps, or has enhanced binding to host cells through a yet-unidentified viral receptor.
Finally, a recent ChIP-seq study in mouse primary fetal erythroid cells showed that a TAL1 mutant that has lost its E-box-mediated DNA-binding activity can still be recruited to one fifth of TAL1 targets, and TAL1 and GATA1 cooperate to stabilize each other at these sites (Kassouf et al, 2010).
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