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In this report we have minimized the background genetic differences outside of ICOS surface expression by using littermate ICOS+/+ and ICOS+/− mice; thus any defects observed are due to differences in this specific costimulatory pathway and not background genetic differences.
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For each adaptor candidate, we tested three different siRNAs per target to minimize the chance that any endocytic defects observed are due to an off-target effect of a particular siRNA sequence.
Linking the synaptic defects observed in Sema5A mutants to the observed behavioral phenotypes is difficult.
Nrp1 Sema− mice mimicked the neural defects observed in the Nrp1 −/− but did not exhibit any vascular abnormalities.
However, our initial attempt using isogenic GLIS3−/− hESCs failed to recapitulate the defects observed in Glis3−/− mice20.
Moreover, SIRT6-depleted cells exhibit abnormal telomere structures that resemble defects observed in Werner syndrome, a premature ageing disorder.
Collectively, the severe hematopoietic defects observed in Mx1-cre/Flox-Apc mice suggest an important role for APC in the maintenance of the hematopoietic stem and progenitor compartments.
Our initial attempt using isogenic GLIS3−/− hESCs failed to recapitulate the defects observed in Glis3−/− mice20, which might be due to lack of GLIS3 expressing cells.
Defects observed in the intestine of CF animal models include deficient anion transport, mucus accumulation and goblet cell hyperplasia in most cases.
This is consistent with our hypothesis that reduced cytosolic EC Ca2+ oscillations account for the angiogenic defects observed caused by tmem33 knockdown.
The elongation defects observed in mutant spermatids can be directly tied to altered postmeiotic chromatin architecture.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com