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In mammalian cells, tension spatially separates centromeric cohesin from Sgo1-PP2A, perhaps leading to loss of protection (Lee et al., 2008).
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The study found that UCP1's activity is directly tied to the increase in cell tension.
Deformation-induced exposure of cryptic sites, defined as buried molecular recognition sites, in FN has been proposed as a mechanism by which cell tension drives FN fibrillogenesis.
Thus, we speculate that the stretch-induced increase in cell tension is responsible for matrix-bound vegf isoform production.
However, current understanding of YAP/TAZ remains limited due to the unknown interaction between the canonical Hippo pathway and cell tension.
In this thesis, I set out to define the molecular biophysical mechanism by which cell tension application at the RGD site promotes unfolding and thereby induces FN-FN self-assembly leading to matrix fibril formation.
In conclusion, loss of FPC disturbs adhesion signaling, cell-cell interaction, and control of cell tension resulting in impaired epithelial morphogenesis, which can be rescued by transient reduction of cell contractility.
So they disrupted cell tension by dabbing immature cultures with a chemical that dismantles the support beams inside; sans chemical, the cultures developed mostly into bone cells, but the treated cultures turned into fat cells.
Importantly, this indicates that the response of contraction rate is specifically due to a change in stiffness and not the cell tension or height.
Even though the absolute cell tension was greater later during contraction, the traction rate was dependent only on the instantaneously applied stiffness (and similarly for cell height and contraction velocity).
As suggested by the reviewers, the best way to quantify cell tension is by laser ablation.
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