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For instance, the cardiac and/or GI defects manifest at around E12.5 (Myh6), E11.5 (SM22α) or E18 (Myh11) in congenital KOs, whereas the GI defect manifests at around 13 14 (SM22α), or 21 days (Myh11 in this study) after tamoxifen injection in the inducible KOs.
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The former also showed a spatial defect since GUS staining could occur in quite different positions and with variable extension.
Results similar to Figures 6A and 6B were observed using additional transgenic lines (DIR1pro DIR1-GUS/ DIR1pro DIR1-GUS/5 and 35S: DIR1Δ1-25-GUS/ dir1-1 lines 17, 20) providing evidence that expression of DIR1-GUS or DIR1Δ1-25-GUS restores the SAR defect in the dir1-1 mutant.
In light of the molecular lesion found in CS3227, we re-examined the circadian defects present in CS3227 alongside the weak gi allele gi-1 and the strong alleles gi-2 and gi-201.
Mutants with auxin-response defects, such as tir1 and axr1, show increased reporter activity after induction and reduced destabilization of AXR3NT-GUS upon auxin treatment [ 16], consistent with the axr1 defect in accumulating normal levels of auxin-responsive transcripts following auxin treatment [ 45, 46].
Gotta Defect!
The Oscars (gi gi gi)!
pi ≈ pio + (gi -dipio Δt.
Heater defect?
Expression of DIR1 without its ER signal sequence rescued the SAR defect in dir1-1 thethe same extent as the entire protein (DIR1pro DIR1-GUS/ DIR1pro DIR1-GUS/
The conditional pdf of X gi given y gi and w gi is given by f (x gi | y gi, w gi ; θ ) = f (y gi | x gi ; θ 1 ) f (w gi | x gi ; θ 2 ) f (x gi ; θ 3 ) ∫ f (y gi | x gi ; θ 1 ) f (w gi | x gi ; θ 2 ) f (x gi ; θ 3 ) d x gi.
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