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We sought to use this newly developed ex vivo system as a novel tool to generate cell models expressing a human frataxin cDNA carrying pathogenic missense mutations.
In the present study, we generated mouse and fly models expressing a form of MGS resistant to inactivation, in which nine regulatory serine residues were mutated to alanine.
The models expressing a heterozygous mouse JAK2V617F all had a PV-like phenotype, whereas the model expressing heterozygous human JAK2V617F was associated with ET with a low-level progression to PV and myelofibrosis.
While the design of our study cannot establish a cause-and-effect relationship between the prolonged elevation of β-catenin and the development of equine EGT, transgenic mouse models expressing a stabilized form of β-catenin in mesenchymal cells develop hyperplastic cutaneous wounds [ 11].
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Here, we generated mouse and fly models expressing an active form of GS to force neuronal accumulation of glycogen.
Models express a rich internal pluralism (see also de Chadarevian and Hopwood 2004; Morgan 2012).
Of note, these models express a constitutively active allele of HRAS, which is not the most common CS-causing allele of HRAS, which is just strongly activating (Sol-Church and Gripp, 2009).
The findings from these two transgenic lines were not replicated when reducing Fyn expression in a different AD model expressing a tau transgene, in addition to APP and Presenilin 1 (3xTg-AD) [ 66].
The problem is then to organize the relationship between an initial abstract state-based model expressing requirements and a final concrete state-based model expressing a structured algorithmic state-based model.
To address this, we have used array tomography to examine an rTgTauEC mouse model expressing a P301L human tau transgene and a transgene labeling cytoplasm red (tdTomato) and presynaptic terminals green (Synaptophysin‐EGFP).
Here, we generated a knock-in mouse model expressing a mutation that abolishes the ankyrin-G/GABARAP interaction (Ank3 W1989R) to understand how ankyrin-G and GABARAP regulate GABAergic circuitry in vivo.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com