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It has the potential to change the current environment of mouse work, providing guidelines for standardized broad-based mouse phenotyping and quality control measures.
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In summary, the present work provides a new mouse model of GD and identifies a previously unsuspected binding of ADAMTSL2 to FBN2, and effect on FBN2 assembly.
To conclude, this work provides a preclinical model of mice prone to MS. IR establishment in TP53INP1-deficient mice is favored by chronic oxidative stress, which drives LD accumulation.
This work provides an example of transgenic mouse imaging to phenotype lymphovascular disorders that might be linked to hereditary lymphatic disorders in humans.
Together, this work provides evidence that primary cultures of postnatal TH-EGFP mice currently represent an excellent model to study the properties of these cells in culture.
This work provides a new non invasive index to predict liver fibrosis induced in mice.
Together with our detailed characterization, this work provides a valuable gene discovery resource for the craniofacial community, and a rich source of mouse models for further investigation.
In conclusion, our work provides multiple lines of evidence that the non-neural developmental defects in Gad1 and Viaat mutant mice are due to a requirement for GABA signaling in the CNS during mouse fetal development.
Our present work provided evidence that (PhTe 2 can elicit several histological abnormalities in liver, kidney, and lung of adult mice.
The work provided some basic and detailed data, which might be referred when further evaluating innate and adapted pulmonary immune responses and local viral load in mice.
Daisy Dunne assisted with mouse work.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com