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To evaluate the role of RIPA in viral pathogenesis, we engineered a genetically targeted mouse, which expressed a mutant IRF-3 that was RIPA-competent but transcriptionally inert; this single-action IRF-3 could protect mice from lethal viral infection.
Experiments were also performed in the GAD67-GFP mouse which expressed GFP fluorescence in some Type III taste cells.
Bnc1 mice were obtained by mating the Bnc1 (+/fl-neo) with a ZP3-Cre mouse, which expressed Cre recombinase only in the oocytes [35].
The 7265PDA cell line was isolated from a pancreatic adenocarcinoma of a mouse, which expressed the KRASG12D oncogene and in addition the p53R172H allele in the pancreas (Pdx1-creER induced expression of the two alleles).
Another method for bioluminescence of migration of endogenous neural stem cells was adopted by Couillard-Despres et al. [ 87], who created a transgenic mouse, which expressed luciferase under the control of the doublecortin promoter, a protein expressed by migratory neuroblasts of the SVZ.
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To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors.
The objective of this study, is to elucidate the in vivo immunomodulatory role of IFN-I signaling in T cells during EAE using a novel transgenic mouse, which expresses functional type I IFN receptor (IFNAR1) exclusively on T lymphocytes (IFNAR1Texcl).
We showed that a well-characterized Foxp3gfp reporter mouse, which expresses an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background.
We then tested these "conditional AAVs" (AAV-LS1L-GFP; AAV-LS2L-RFP) using two different Cre knockin drivers, the Pv-cre mouse, which expresses Cre in parvalbumin-containing (PV+) GABAergic neurons [23], and the Emx-cre mouse, which expresses Cre in glutamatergic neurons in the forebrain [24].
Finally, transgenic mouse models have been engineered to mimic celiac disease, most notably the NOD Ab° DQ8+ mouse, which expresses human DQ8 in an endogenous MHC class II-deficient (Ab°), autoimmune-prone (NOD) background [36].
For comparison, we included sections of an age-matched female FDD-Tg mouse, which expresses the Danish mutant form of human BRI2 under the mouse prion protein promoter [20].
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