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The mutations behaved in a non-canonical fashion in complementation tests, forming what Ed Lewis called a "pseudo-allelic" series.
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The minigene carrying the mutation behaved in an identical manner (Lane 2).
We previously reported that Δ5G, a SIVmac239 molecular clone with quintuple deglycosylation mutations behaved as a live-attenuated virus in vivo [2], [3].
Neither the AFG nor K1009X mutations behaved as modifiers, although AFG had a variable weak effect.
Partitioning nonsynonymous and silent SNPs according to their frequency, we estimated that 23% of amino acid changing mutations behave as neutral in O. edulis, which is similar to the estimates obtained in humans and the common fruit fly [20% and 24%, respectively (Fay et al. 2001; Shapiro et al. 2007)].
As a general effect and in agreement with previous reports, most mutations behave as flexibility amplifiers which favors the access to otherwise impeded states [19],[30] [32].
The data suggest that mutations are acquired in a lifelong random manner, and that most mutations behave as neutral 'passengers' at HSC level until an additional 'driver' mutation supports clonal amplification of a subset of passenger mutations (Welch et al., 2012).
'Latent driver' mutations behave as passengers, and do not confer a cancer hallmark.
Then, these evidences suggest that mutations behave as effectors for the definition of possible interactions sites.
In the case of KCNC3 and SPTBN2, we have shown that the mutations behave as dominant negatives and both of these affect channel function, directly or indirectly.
Likewise, a G210A mutation behaved like wild-type Wnt3a in the Wnt reporter assay (data not shown).
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CEO of Professional Science Editing for Scientists @ prosciediting.com