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The ability of this altered epigenome to promote a transgenerational epigenetic alteration in the transcriptome has been shown in the developing testis [13] and is speculated to be the mechanism behind the subsequent development of heritable adult onset disease [3], [6].
It was recently shown in the developing central nervous system (CNS) that TSPs promote the formation of new synapses, which are the unique cell-cell adhesions between neurons in the brain.
In a recent publication it was shown in the developing heart that TGFB2 modulates Has2 expression and HA production with subsequent induction of epithelial to mesenchymal transformation [32].
Additionally, it has been shown in the developing limb that Notch signaling can induce Hes/Hey gene expression.
The dependence of neurite outgrowth and elongation on p53 has also been shown in the developing cerebellum.
Disparities between mRNA and protein levels of the NR2A subunit were also shown in the developing visual cortex (Cao et al. 2000).
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However, to our knowledge, these steps have not yet been shown in the living, developing brain and the underlying types and roles of growth cone dynamics are unknown.
TLR9 is involved in autoantibody production, as shown in the model developed by Leadbetter and colleagues [ 34], and probably but indirectly in inactivated DNAse mice [ 35].
Recent studies have shown that in the developing embryo, arterial and venous identity is established by genetic mechanisms before circulation begins.
For example, it was recently shown that in the developing tracheal air sac of Drosophila larvae, matrix metalloprotease Mmp2 spatially restricts FGF signaling [32].
Also, a recent study has shown that in the developing mouse retina, notch2 is expressed in progenitors and Müller glia (Zhu et al., 2013), an expression pattern that is reminiscent of that for mdka in the developing zebrafish.
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