Sentence examples for mouse vascular development from inspiring English sources

Exact(5)

As in mouse vascular development Rudhira/BCAS3 is expressed transiently in differentiated human endothelial cells during human vascular development.

We set out to use this technique to study the normal sequence of mouse vascular development between E8.0 and E10.0.

AVS similar to the DA-CCV shunts have been noted in the course of normal embryonic mouse vascular development connecting the primordial ACV directly to the DA, anterior to the first somite [44].

Instead, impaired ISV extension is likely caused by a cell-autonomous defect in endothelial cells deficient in NRP1, as observed for mouse vascular development (Fantin et al., 2013a).

As FAK is required for normal mouse vascular development, as well as pathological angiogenesis, (Ilic et al., 2003; Shen et al., 2005; Braren et al., 2006; Lee et al., 2010; Tavora et al., 2010) we were interested to determine if human endothelial cells required FAK for complex angiogenic functions such as morphogenesis.

Similar(54)

We describe examples of vascular remodelling that provide new insight into the mechanisms of sprouting angiogenesis, vascular guidance cues and artery/vein identity that directly relate to phenotypes observed in mouse mutants affecting vascular development between E8.0 and E10.0.

VEGFR3-deficient mice die of defective vascular development before the lymphatic system becomes established [ 10].

In vitro studies of para-aortic splanchnopleural explants showed that AML-1-deficient mice also exhibit defective vascular development (Takakura et al, 2000).

Defects in mesoderm, neural tube and vascular development in mouse embryos lacking fibronectin.

During retinal vascular development in mouse, wild-type ECs can instruct Fz4 −/− ECs to assemble into mosaic vessels, suggesting that Wnt/β-catenin signaling (Wang et al., 2012) is not a uniform requirement for all ECs during vascular network formation.

Here, we have combined the analysis of vascular development in the mouse hindbrain with functional studies in primary human ECs, zebrafish embryos, and mouse retina to demonstrate that NRP1 is dispensable for the genetic specification of tip cells but essential for CDC42 activation.

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