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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.
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.
However, current understanding of YAP/TAZ remains limited due to the unknown interaction between the canonical Hippo pathway and cell tension.
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.
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Biophysical and Molecular Determinants in Cell Tension-Mediated Fibronectin Unfolding that Drive Fibrillogenesis.
It was notable that the IST1R 4SA could also still support abscission delays when the checkpoint was induced by low-cell tension.
In mammalian cells, tension spatially separates centromeric cohesin from Sgo1-PP2A, perhaps leading to loss of protection (Lee et al., 2008).
Using single-cell force spectroscopy they have measured the cell-cortex tension of these cell types (ectoderm, mesoderm and endoderm) while specifically interfering with actomyosin-dependent cell-cortex tension.
Chugh, P. et al. Actin cortex architecture regulates cell surface tension.
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