Sentence examples for mice also generated from inspiring English sources

H50Gmu(a) Tg mice also generated memory B cells.

Activation of MYC in Rb deficient mice also generated significantly more 4n hepatocytes compared to loss of RB alone.

Similarly, transmission of Mi PrPSc, i.e., p-dCJD, to the 129 M/M mice also generated Mi PrPSc.

Indeed, transmission of sCJD-MV2K containing Mi PrPSc and V2 PrPSc to the 129 M/M mice also generated Mi PrPSc.

Splenic FO B cells from λ5 KO mice also generated ∼fourfold more ASC whose antibody was reactive with PC compared to wild-type splenic FO B cells (Fig. 6A).

TCR transgenic (TCR-Tg) mice were also generated, in which mice more than 90% of the CD4+ T cells expressed the V α1.1 and V β4 chains recognizing dominant and possibly most arthritogenic "5/4E8" T cell epitope (see above in Section 7) [ 4, 113].

In addition to cartilage-specific PPARγ KO mice, we also generated inducible cartilage-specific PPARγ-mTOR double KO mice to specifically dissect the in vivo role of mTOR pathway in PPARγ signalling during OA.

To evaluate whether miR-34c and the other 4 members of the miRNA family have an essential role in the first cleavage division both in vivo and in vitro, we analyzed miR-34b/c (Choi et al., 2011) and miR-449 (Bao et al., 2012) knockout mice, and also generated miR-34b/c; miR-449 double knockout (herein called miR-dKO) mice.

Cre positive, ARflox negative mice were also generated to confirm that expression of Cre alone did not induce a phenotype [8].

Safb1-null mice were also generated by homologous recombination and had a deletion of exons 7 through 22 [ 26].

+/Cre mice were also generated by mating Fabp4-Cre stud males to C57BL/6J females to confirm that expression of Cre alone did not induce a phenotype.