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This establishes a role for FLNs in migration and suggests that compensation by other FLN isoforms [25] may mask the migration phenotype in single knockdown cells or single knockout cells or animals.
Therefore, we tested for enhancement of the DTC migration phenotype in worms exposed to various stresses.
Therefore, it necessitates a careful examination of coordinated Rac1-RhoA signaling pathways to predict the final migration phenotype in IAP-depleted cells.
Interestingly, MAPK signaling contributed to the migration phenotype in the Cdc42GAP knockout neutrophils, which showed changes in ERK and p38 phosphorylation that were similar to those detected in the Cdc42-overexpressing mammary glands.
The most prominent DTC migration phenotype in cacn-1 RNAi animals is one in which the cells fail to stop migrating at the end of L4, bypassing the correct stopping point opposite of the vulva (Tannoury et al. 2010).
Our observation of stable-bleb cell extrusion from tissue explants along with observations of a similar migration phenotype in various cancer cell lines (see Liu et al., 2015) also points at the intriguing possibility that stable-bleb cells might be involved in other contexts such as cancer metastasis where cancer cells disseminate from the primary tumor into unaffected tissues.
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Recent research has identified different migration phenotypes in 2D and 3D [2], [20] [20].
We suggest that the lack of overt migration phenotypes in many FLNa-deficient cells and organisms is likely to be due to the presence of co-expressed FLNb, or FLNc, which is able to compensate for the lack of FLNa, and that in some cases the plasticity of tissue development may accommodate the delay in initiation of cell migration caused by loss of FLNa.
Some unc-34 gm104);wsp-1(RNAi) unc-34 gm104lay wsp-1 RNAiration wsp-1 RNAi, in which all cembryosentually reach the midisplay
The cell lines with high and moderate expression of laminin-5γ2 displayed stronger migration phenotypes in trans-well test than those with negative expression of laminin-5γ2 [ 15].
Additionally, while I appreciate the lack of migration phenotypes in other KOs examined here, contrasted with Asada's manipulations of LKB1, I am concerned about the extent of the loss of function induced.
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