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One example are the Tail-short (Ts) mutants of laboratory mouse strains; these mutants have short, kinky tails and numerous skeletal abnormalities.
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Since both Gja3 (α3 connexin) and Gja8 (α8 connexin) knockout mice were originally generated from J1 ES cells of the 129SvJae mouse strain, these mutant mice probably had 129SvJae alleles on chromosomes 14 and 3 where Gja3tm1 and Gja8tm1 are located, respectively.
Furthermore, in backcrosses with the C57BL/6J (B6) mouse strain these episodes are much more prolific than in the HeJ parental strain suggesting that modifier genes regulate the incidence of SWD (32).
For most of these mouse strains, the major factor that predisposes the mice to mammary tumours is the presence of the MMTV.
Because the environmental conditions in these experiments can be controlled, any differences observed between the mouse strains in these phenotypes most likely can be attributed to genetic differences.
IGFBP3 and Epo have both been shown to support endothelial cell survival and mouse strains lacking these factors displayed increased hyperoxia-induced vessel loss [46], [47].
It is, however, possible to use all 3 mouse strains in these homing experiments since the time span examined are relatively short as to avoid an immune response from the immune competent mice towards the xenotransplanted EOCs.
We subjected genetically diverse mouse strains to these tests, including 10 wild strains (BFM/2Ms, PGN2/Ms, HMI/Ms, BLG2/Ms, NJL/Ms, KJR/Ms, SWN/Ms, CHD/Ms, MSM/Ms and CAST/Ei), a fancy strain (JF1/Ms) and 6 standard laboratory strains (C3H/HeNJcl, CBA/J, BALB/cAnNCrlCrlj, DBA/2JJcl, 129 +Ter/SvJcl and C57BL/6JJcl).
Therefore, to test whether our initial observations were limited to these mouse strains or whether these traits are common across rodent species we have tested additional strains of mice (CBA/J and AKR/J) and rats (Sprague Dawley).
The extent to which variance between mouse strains (on which these estimates are based), may be impacted on by factors pertaining to litter or maternal rearing differences is beyond the scope of this study.
Consistent with our findings, mouse strains in which these genes are deleted show ataxic phenotypes.
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