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PI16-deficient mice were engineered and found to generate higher levels of processed chemerin than wildtype mice.
Transgenic (TG; FVB/N background) mice were engineered to express rat CRNK under control of the α-myosin heavy chain promoter, and crossed with FVB/N mice with cardiomyocyte-specific expression of caPKCε to create double TG mice.
To compare CD40 and LMP1-mediated events in vivo, transgenic mice were engineered to express mouse CD40 (mCD40tg) or a protein with extracellular mCD40 and cytoplasmic LMP1 (mCD40-LMP1tg).
The mice were engineered so that their cancer cells overexpressed MUC1, just like human cancer cells do.
Accordingly, when transgenic mice were engineered to express the rat Mup their kidneys developed the disease.
These transgenic mice were engineered to over-express in B lymphocytes a TRAF2 mutant that mimics TRAF1 and the anti-apoptotic protein Bcl-2.
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APP transgenic (TgAPP) mice are engineered to overexpress human APP, and in most cases exhibit Aβ-dependent pathology and cognitive deficits.
Such transgenic mice are engineered to express human APP transgenes containing mutations known to cause autosomal dominant, early-onset AD, and are widely used for preclinical drug screening in AD.
Svante Paabo, in whose laboratory the mouse was engineered, promised several years ago that when the project was completed, "We will speak to the mouse".
For example, a mouse was engineered to carry a duplication of genes corresponding to a region of chromosome 15, the location of the most frequently observed chromosomal abnormality in ASD.
A mutant mouse was engineered to harbor two amino acid substitutions (S270H, L277A) in the GABAA receptor (GABAA-R) α1 subunit; this mutation abolished sensitivity to the volatile anesthetic isoflurane in recombinant GABAA-Rs, and reduced in vivo sensitivity to isoflurane in the loss-of-righting-reflex assay.
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