Sentence examples for mouse strain where from inspiring English sources

Here, we devised a new approach and engineered a single mutant mouse strain where the endogenous Ctgf-3' untranslated region (3'UTR) was replaced with a cassette containing two 3'UTR sequences arranged in tandem.

As this previous work used a transgenic mouse containing a BAC with the Ascl1 coding region replaced by CreER™, we reexamined this issue with an Ascl1CreERT2 knock-in mouse strain where CreERT2 replaced endogenous Ascl1 (Fig. 2A) such that CreERT2 is restricted to Ascl1 expressing cells (Fig. 3E–E').

This mutation originated in the highly inbred B6 mouse strain, where it leads to consistent pigmentation defects in otherwise normal heterozygotes (primarily a white belly "splotch").

We track the fate of RGS5+ pericytes in response to focal ischemic brain injury using a knock-out/knock-in mouse strain where GFP is expressed from the Rgs5 locus.

In order to generalize our in vitro findings, we also investigated the role of NF-κB in vivo after prion infection of Nfkb1 /–, Nfkb2 /– and Bcl3 /– mice and a mouse strain, where p65 (RelA) was deleted in the central nervous system (CNS).

Gene structures were transferred using exonerate's (62) cdna2genomodeldel to align transcripts between the C57BL/6J and NOD mouse strains where clear homology existed and verified.

The observed ∼4 hr peak-to-peak spacing is in line with a previous study on several circadian competent mouse strains where ultradian rhythms with similar period length were detected (Dowse et al., 2010).

F1 hybrids were generated by reciprocally crossing C57Bl/6J and Cast/EiJ mouse strains, where we denote by F1i an F1 hybrid derived from a C57Bl/6J father and a Cast/EiJ mother, and by F1r an F1 hybrid derived from a Cast/EiJ father and a C57Bl/6J mother.

In general it requires analysis of embryogenesis of mutant mouse strains where regular arrangement of sensory hair cells in the inner ear and neural tube closure phenotypes are the most commonly used readouts for PCP-like signaling in mammals [ 7, 8].

Thus the TGFB2 gene was identified as a candidate gene to CM susceptibility in a genetic cross that used wild-derived mouse strains and where CM susceptibility segregated from hyperparasitaemia [42], suggesting that TGFB2 would be a gene conferring risk to CM in the context of severe malaria.

These results were subsequently confirmed in a second mouse strain, namely NSG mice, where tumor growth was observed with 105, 104 and 103 (one out of three mice) injected sphere cells, but only with 106 adherent cells (Figure 1D).