Sentence examples for mouse retinal development from inspiring English sources

Genes that correlated with more than three seed genes were investigated for potential biological relevance in mouse retinal development.

ISH confirmed the expression of Ect2 in subsets of cells in the ONBL across the three stages of mouse retinal development (Figure 6E G).

Traditional wet-lab experiments will be required to test these hypotheses of the specific role of each candidate gene and its placement in the gene regulatory network during mouse retinal development.

To understand the functional significance of LMO4 in mouse retinal development, we conditionally ablated a floxed LMO4 allele in the retina using the Pax6 alpha enhancer driven Cre recombinase [8].

Despite the morphological and developmental disparity of the fly compound eye [8], [9] and the mouse camera-type eye [10], [11], gene conservation during both fly and mouse retinal development is well-documented [12] [16] and there is an implicit assumption of gene regulatory network conservation as well [17], [18].

Based on the evolutionary conservation of gene relationships, we test the hypothesis that a seed network derived from studies of retinal cell determination in the fly, Drosophila melanogaster, will be an effective way to identify novel candidate genes for their role in mouse retinal development.

The majority of our candidate genes were correlated (positively or negatively) with the same three seed genes (Notch1, Eya1 and Six3) suggesting that these three seed genes are at the functional core of this network regulating retinal development in mouse.

Our results also support the second hypothesis that the mouse network derived from relationships between homologous genes from the fly RDGN (i.e. our extracted seed network [ESN]), would be an effective way to discover high quality candidate genes involved in retinal development in mouse.

The depletion of TUG1 in the developing mouse eye was found to block retinal development.

We also sought to compare Rb family expression and intrinsic genetic compensation during retinal development in mice and humans to explain why humans are susceptible to retinoblastoma following RB1 inactivation, but mice are not.

NRP1 lacking the C-terminus three amino acids [Ser-Gln-Ala (ΔSEA)] led to impaired vasculogenesis in zebrafish (Wang et al., 2006) and abnormal vascular remodeling during retinal development in mice (Fantin et al., 2011).