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This model will be a founder mouse for forward genetics of autistic disease and an invaluable tool for its therapeutic development.
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The GhrR KO animals used in these studies were bred from a single founder mouse at the Charles River Laboratories (Wilmington, MA) [ 28].
A BALB/c deaf14/deaf14 founder mouse was crossed to a C57BL6+/+ mouse and the offspring intercrossed.
PCR was used to identify founder mice, which were bred with mouse mammary tumor virus-reverse tetracycline transactivator mice (MMTV-rtTA) [ 16] already in use in our laboratory [ 17].
A chimeric male founder mouse was generated and crossed to normal C57BL/6 mice to generate heterozygous mice containing one copy of the mutated EpCAM allele.
The founder mouse was discovered 50 years ago in a litter from a C3H/HeJ colony because of its unexpected yellow coat [ 20].
Germline heterozygous alleles were generated by crossing founder mice carrying the R120G mutation on one allele with C57BL6 mice.
The neomycin (Neo) selection cassette flanked by Frt sites was removed by crossing founder mice (Ptbp2 Neo-loxP/+) with 129S4/SvJaeSor-Gt ROSA 129S4/SvJaeSor-Gt ROSAce (Jackson) carrying Flp recombinase.
One transgenic founder mouse was obtained and bred to establish a transgenic mouse line.
As a first step to produce homozygous β+IVSI-6 transgenic lines, the founder mouse was back-crossed with wild-type mice.
In addition, we observed 4 cases of obesity (>40 g) during old age, 3 of them were founder mice and included the founder mouse for line B (which we selected for further analysis based on high TG expression levels) and 1 was an F1 TG mouse of line B. Finally, C57BL/6 mice are genetically predisposed to hydrocephaly (1 4%), we observed 2 cases in NTG mice and none in TG mice.
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