Sentence examples for murine knockout models from inspiring English sources

Several murine knockout models revealed that development and differentiation of these cells are controlled by transcription factors; and one of the major regulators is the CCAAT enhancer binding protein (C/EBP) family.

Deletion of the gene encoding Sclerostin (Sost) causes a rare sclerosing bone dysplasia, sclerosteosis (OMIM ID 269500) in both humans and murine knockout models [30], [31], [32], [33]; a related disease, van Buchem's disease (OMIM ID 239100), is caused by a distal noncoding deletion that removes regulatory elements required for the transcriptional of the Sost gene in adult bone [32].

Murine knockout models of arthritis which can sequentially test the function of the identified members of clotting pathways could also be used to verify this hypothesis.

Evidence from murine knockout models using leptin-deficient mice has shown an increased intestinal mucosal permeability and portal endotoxaemia in genetically obese mice [ 26].

Similarly, murine knockout models have identified TGF- β and TNF- α signaling in gap junctional alterations observed in T. cruzi infection.

These targets have been previously identified, based on murine knockout models or significant associations between biomarker data and adverse pregnancy effects, as critical to proper embryonic blood vessel formation or maternal fetal placental circulation.

Second, the lack of prominin-1 in a murine knockout model leads to complete disorganization of the outer segment early in postnatal development ending with the complete loss of the outer nuclear layer (ONL) in older animals [12].

Finally, analysis of peripheral blood from normal persons and a WAS patient with a revertant mutation indicates that key observations derived from the murine knockout model mirror the role for WASp in human B-cell function.

While our in vitro studies support a role of OCRL in ciliary function, the lack of phenotype in the murine knockout model can be interpreted in the context of the primary cilia and polarity dysfunction (71).

Using a murine CD177 knockout model, the present study demonstrates that CD177 plays a crucial role in neutrophil viability, but has no impact on chemotaxis.

As an addition to the present study it would be interesting to study liver cirrhosis in the established murine A1R knockout model.