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H2O2 can facilitate cross-linking of cell walls [ 39], and callose (β-1,3-glucan) deposition may reinforce cell walls at contact sites with fungal structures.
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This work highlights Smad4 as a point for signaling crosstalk in the TGF β cascade: it is tempting to speculate that during Xenopus mesoderm development, Dvl and Par1b activity may couple and reinforce cell fate specification triggered by TGF β ligands with cell polarization and migration.
Pectinesterases demethylate pectins and make them more susceptible to polygalacturonase action [ 38], but they may also reinforce cell-to-cell adhesion [ 39].
Thus, miRNAs may not be critical in the earliest stages of trophectoderm specification, but rather, may serve as developmental modulators that reinforce cell fate specification at later points in the differentiation process.
Furthermore, Foxa2 genetically interacts with a number of other transcription factors (i.e. Noto [ 91], Lhx1 [ 92], Otx2 [ 93], Gsc [ 94]) and further investigation may reveal that feedback loops work to reinforce cell fates in these contexts as well.
Cytokines acutely released by these cells (including T cells) may reinforce or amplify microglial activation but abundant Fas Ligand [39] and other inhibitory factors in the CNS attenuate subsequent steps of the adaptive response and prevent a classical CsA-sensitive T cell amplification and cytolytic graft rejection.
The fact that RA synovial lining cells express α5β1 and αvβ3 integrins [ 50- 52], however, suggests the possibility that ADAM15 may function as a binding molecule to reinforce cell-cell and/or cell-ECM interactions.
Since Nanog is an important pluripotency factor, it is highly likely that the overexpression of Nanog in ESCs may reinforce the pluripotency regulatory circuit, or stem cell properties, of ESCs.
These shared methylation signatures may reinforce the hypothesis of basal-like tumors arising from a mammary stem cell and progressing to differentiated cells with more luminal characteristics (HER2 enriched, luminal A and B).
Many of the impacted splicing events are part of an epithelial splicing program, suggesting that effects of Msis on splicing may reinforce the effects of Jag1 repression on maintenance of epithelial cell state.
The presence of H3K9Me3, however, may reinforce gene silencing and promote the heritability of chromatin changes during cell division.
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