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In addition, we show that CHD4 acts as an important regulator of the G1/S cell-cycle transition by controlling p53 deacetylation.
The miR-200 family plays a crucial role in epithelial-to-mesenchymal transition by controlling cell migration and polarity [ 106– 108].
Axin2 can regulate epithelial-mesenchymal transition by controlling Snail1 activity in breast cancer cells (Yook et al, 2006) and its expression has been shown to be upregulated in breast tumours (Ayyanan et al, 2006).
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Finally, CHD4 depletion leads to defects in the G1 to S transition, probably by controlling deacetylation of p53, and in the G2/M checkpoint upon DNA damage [ 128- 130].
The results of this study also offer possibilities of improving the lithium storage capacity of transition metal oxides by controlling both architecture and composition.
In our study, both Hsp90 and Hsp73 exhibited a clear-cut expression in mitotic cells: Hsp90 seems to regulate the metaphase-anaphase transition [ 55], by controlling the stability of the centrosomal Polo kinase [ 56], whilst Hsp73 appears to be localized on the fibres of spindles and asters during metaphase [ 57].
Collectively, these results indicate that xylitol, like glucose, acts specifically on endocrine cell development, by controlling the transition between Neurog3 and NeuroD.
In summary, our findings support the hypothesis that, from mid-neurogenesis, Sall1 promotes terminal neurogenesis of PCs, initially by controlling the transition from an RGC to an IPC and later by regulating terminal neurogenesis of IPCs.
Degradation in bacteria might also be regulated by controlling order disorder transitions.
The robust TiC transition layer was formed in-situ by controlling the interface reaction and diffusion process between the deposited Ti layer and the SiC matrix.
Its product, pRb, inhibits cell proliferation by controlling the G1/S transition.
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