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A study of hippocampal gene expression in eight mouse strains reported >200 genes showing strain differences (Fernandes et al. 2004).
Similarly, a study of several inbred mouse strains reported that head-dipping and locomotion are highly correlated (Kliethermes and Crabbe, 2006b).
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Neither knockout mouse strain was reported to develop spontaneous disease.
This mouse strain is reported to be diabetes and obesity resistant due to a greater amount of active BAT (3).
Furthermore, identical respirasome organization was observed using the BALB/c mouse strain also reported to be homozygous for the Cox7a2l short allele.
This mouse strain was reported in 2002 (Levanon et al, 2002) and their properties of Rehovot-Runx3 KO were later described as follows: This genetic modification did not result in a Runx3-null allele since the p33 Runx3 splice variant escaped the knockout strategy (Supporting Information Fig S1, upper left panel; Fainaru et al, 2004 ).
Furthermore, no changes in ventricular volume or anatomical features of two different AQP4-null mice strains were reported [ 143].
Studies using the mouse adapted Fujisaki prion strain reported white matter destruction and deposition of abnormal PrP in white matter tracts [ 8, 27], without being more specific regarding the PrP deposition pattern.
Here we report that LPS resistance of the inbred mouse strain SPRET/Ei, previously reported to depend on the glucocorticoid receptor (GR), maps to the distal region of the X-chromosome.
Genetic polymorphisms across mouse strains have been previously reported for the Wap gene.
The following previously reported mouse strains were used in this study; Tln2KO (Tln2tm1.1Crit) where Tln2 coding exon1 is deleted [12]; Tln2sgt (Tln2Gt(S1-6D1)Sor) with a gene trap insertion upstream of the first coding exon [2,13]; Tln2Gt RRI434 BygRI434)Byg) with a gene trap insertion between coding exons 28 and 29 [2913].
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