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KLF15 has previously been shown to be capable of inhibiting the rhodopsin promoter [97], [98], but otherwise, no function has been ascribed to these factors during murine retinal development.
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In this study, we sought to determine if IL-10 affects murine retinal neovascularization during postnatal development, the cause of blindness in infants with ROP.
Vascular development in the early embryo is difficult to observe, but the murine retinal vascular system develops after birth and is therefore easier to examine.
It is also associated with embryonic stem cell-derived neural progenitors [21], and importantly, it is detected along the former ventricular zone of the developing midgestation murine retinal primordium containing neuroepithelial progenitors well before retinal histogenesis takes place [7], [18].
Several large-scale gene expression studies of the murine retina have been conducted in an attempt to identify genes important for retinal development (Akimoto et al. 2006; Blackshaw et al. 2004; Dorrell et al. 2004; Liu et al. 2006; Mu et al. 2001; Zhang et al. 2006).
The depletion of TUG1 in the developing mouse eye was found to block retinal development.
It has been shown that Nestin is expressed in murine retinal progenitor cells [25].
The presence of such homologs for other genes in the Drosophila neuroblast cascade in subsets of RPCs during mouse retinal development suggests that a cascade similar to that in Drosophila might be playing a role in the progression of competence states in the murine retina as well.
It is reasonable to assume that, like its role in neuronal development, Nestin is essential for the retinal development primarily by controlling the retinal progenitor cell survival.
This spatial resolution is marginally higher than the average receptive field diameter of murine retinal ganglion cells, estimated to be ∼130 um [44] or ∼200 um [47].
Retinal development has long been considered to be insensitive to experience.
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