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Here, we characterise the lens and eyes of the Crim1KST264 mutant mice, and show that the loss of Crim1 function in the ocular tissues results in inappropriate differentiation of the lens epithelium into fiber cells.
Thus, inappropriate differentiation protocols mask differentiation potential.
As many of these genes are key developmental regulators, the current model holds that PcG protein-mediated repression prevents inappropriate differentiation.
These results indicate that PRL expression in the endometrium is a tightly regulated process that is dependent on the coordinated action of multiple transcription factors, which likely acts to canalize decidualization stimuli and ensure inappropriate differentiation does not result from low level or erroneous stimulation of stromal cells.
In summary, we show a complex sequence of events immediately following loss of function of Lkb1 leading to the inappropriate differentiation of secretory cells associated with abnormal expression of Notch pathway elements and consistent with many features of Notch pathway improper regulation.
Neither ArtΔ/Δ nor control cultures showed evidence of inappropriate differentiation.
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Specifically, we found that Mpt5 prevents inappropriate cell differentiation through the inhibition of fMAPK pathway activity.
Moreover, Mpt5 specifically inhibits the output of the pathway in the absence of stimuli, and thereby prevents inappropriate cell differentiation.
The consequence of these signaling changes in the mutants is the inappropriate (ectopic) differentiation of the epithelium into inner enamel epithelium which links (fuses) the adjacent tooth germs.
Deletion of Eset results in a failure to establish the epiblast due to inappropriate trophectodermal differentiation (Yeap et al. 2009).
Interference with NuRD function by deletion of the Mbd3 gene abrogates the formation of a normal epiblast possibly caused by inappropriate trophectodermal differentiation (Kaji et al. 2007).
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