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The paper by Xu et al [ 1] demonstrates one way forward that uses a conditional knockout approach to mutate the intact allele in the mammary glands of mice bearing heterozygous deletions of Brca1.
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On-going studies using a conditional knockout mouse model for Dhs will help us to more clearly differentiate the impacts of DOHH and DHS function in higher eukaryotes.
To test this hypothesis, we used a conditional knockout approach to eliminate E-cadherin specifically in the intestinal epithelium during embryonic development.
Herein, we sought to specifically address the role of Cbfβ in cartilage and bone development by using a conditional knockout (CKO) approach.
Here, we examined T cell and thymic epithelial cell development using a conditional knockout approach.
Using a conditional knockout (KO) mouse model for Cobra1, we demonstrate a critical role of Cobra1 in early embryonic development.
The most appropriate approach to avoid this kind of bias would be using a conditional knockout model.
The requirement of NBS1 for efficient CSR has also been demonstrated by analyzing NBS1-deficient mouse B cells using a conditional knockout strategy [29], [30].
Therefore to analyze the Smad1 function in cartilage we used a conditional knockout strategy to specifically delete Smad1 in the growth plate by crossing mice with a floxed Smad1 allele to transgenic mice carrying Cre recombinase driven by the type II collagen promoter (Col2a1-cre) [25].
We therefore used a conditional knockout allele of Runx1 (Runx1 L/L ) (Li et al., 2006b).
Indeed, data from our laboratory revealed a novel role for Myc in the mammary gland using a conditional knockout approach.
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