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There has also been a mutant mouse strain described (129S5- Prkd3 Gt (OST191038 ) Lex /Mmcd) that harbours a gene-trap deletion of PKD3.
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The targeted deletion of the cystatin C gene was originally made in an embryonic stem cell line derived from the 129/Sv mouse strain, as described previously [ 27].
Panx1−/− mouse strain was described previously [ 29].
The creation of this kidney specific megalin-deficient mouse strain was described in detail previously [ 15].
The ob/ob mutant mouse strain was described as early as the 1950s, 28, 29 exhibiting excess adipose tissue along with impaired reproductive behavior 30 and weighing approximately three times more than normal mice by maturity; however, the ob mutation remained elusive for many years; but in 1994 positional cloning was used to identify and characterize the gene.
Mouse strains are described in Extended Experimental Procedures.
The human DR4 transgenic and the backcrossed B-cell deficient mouse strains were described previously [ 18- 20].
ApoE × GDKO mice were generated by crossing ApoE-KO and GZMB-KO mouse strains as described previously.
Beside the CBA strain, three further mouse strains were described previously as moderately susceptible to rAML: the RF, SJL/J, and the C3H/He strains.
To confirm the relative temporal expression of these two stage-regulated proteins, freshly differentiated L. major Friedlin promastigotes, derived from amastigotes isolated from the lymph nodes of susceptible mouse strains (as described in Depledge et al., 2009), were subject to minimum passage in culture prior to analysis over a time-course.
The c/ebpβ knock-out mouse strain has been described earlier (Sterneck et al, 1997) and the LIP knock-in mice have been generated as described in the Supplementary data.
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