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In this report, we used features of the engineered mice that allowed control of timing of NPC rescue.
In this study, the authors only found slight modifications of single-channel activity in Ser2808-mutated mice that allowed for normal Ca2+ transients and unaltered overall cellular function.
In a landmark paper, Clark et al. (2003) performed the first analysis, via comparisons of sequence data from humans, chimps, and mice, that allowed inference of the positively-selected genetic changes that have taken place along the human lineage.
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Over the past decade severely immune-compromised mice that allow better engraftment of human tissues (such as thymus, liver, bone marrow, and stem cells) have been developed.
Here, we propose a novel and inexpensive system for measuring electroencephalographic signals and other biopotentials in mice that allows for natural movement.
Instead of generating p53 germline mutations, we generated mice that allow global somatic deletion of one or both copies p53 at any chosen time.
Since Smyd2 expression is not restricted to the heart (Fig. 1C), we generated mice that allow the tissue specific deletion of Smyd2 expression.
We applied Cre/loxP system to generate conditional gene targeted mice that allow inactivation of critical components of Notch signaling pathway in the skin.
Therefore, we investigated the development of retinal vasculature by using Sca1-GFP transgenic mice that allow the direct visualization of GFP-positive vascular endothelial cells [11], [12], [13].
To study the function of Notch signaling in the skin of adult mice, we made use of a series of conditional gene targeted mice that allow inactivation of several components of the Notch signaling pathway specifically in the skin.
Together, these data argue for plasticity in the genetic program of peripheral DNCD3 cells from young NOD mice that allows them to differentiate in an extra-thymic environment into mature T-cells with regulatory (anti-diabetogenic) function.
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