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In summary, the 40 and 75 nm nanopore surfaces promoted cell adhesion and migration in fibroblasts by controlling the temporal expression of integrins and ERK1/2.
Doyle et al. observed a coordinated migration in fibroblasts moving on thin (1D) lines with a width of up to 5 µm [1].
Together these results support the idea that p38 MAPK promotes cell migration by upregulating AKT in fibroblasts cultured on native collagen, while p38 MAPK acts as a stress kinase to depress migration in fibroblasts cultured on 3DG-collagen.
Since it has been reported that migration in fibroblasts works best for an intermediate range of Rac activation [27], we titrated iRap concentrations down from 5 µM to 50 nM.
However, more recently, it was shown that both receptors could promote migration in fibroblasts with additive effects when both were present [ 18].
Using genetic disruption in the mouse, we have shown that PDZ-RhoGEF is dispensable for embryo development and a number of known RhoA signaling-mediated processes, including stress fiber formation and cell migration in fibroblasts (Ridley, 2001b).
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However, selective removal of Mena from adhesions did not affect cell migration speed in fibroblasts (Bear et al., 2000).
The results (shown in Figure 5) indicate a slight response of the keratinocytes, but stronger migration activation in fibroblasts, noticeable even after 6 hours in the presence of the highest extract concentration.
siRNA interference experiments show that the AR/FlnA/integrin beta 1 complex controls androgen-induced cell migration in NIH3T3 fibroblasts.
Our results showing defects in cell migration in CEDNIK fibroblasts highlight the importance of membrane fusion mediated by SNAP29 for normal terminal differentiation of the skin.
Moreover, accumulation of progerin has a negative impact on cell cycle progression and elicits reduced migration in HGPS fibroblasts [30], [39].
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