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Using cell based assays they have been implicated in the establishment of cell polarity, cell-shape change, cell migration, phagocytosis, secretion, cell-cycle progression, cytokinesis and transcription [1].
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Thus the cytoskeleton changes, cell migration and invasion, angiogenesis, proliferation and apoptosis, crosstalk pathways linking to Slit-Robo signaling need to be elucidated.
In addition to cell growth, morphological changes, cell migration, and continuous perfusion can lead to changes in matrix fiber arrangement and remodelling that also influence the physical properties of the internal scaffold [ 15].
The results are expressed as fold change in cell migration from upper well to lower well and expressed as neutrophil migration index relative to control, which is kept as 1.
The non-receptor tyrosine kinase focal adhesion kinase (FAK) was found to be co-associated with and highly activated by EphB2 expression, and FAK activation facilitated focal adhesion formation, cytoskeleton structure change and cell migration in EphB2-expressing GBM neurosphere cells.
Since YM583483 did not change basal cell migration, Gβγ-activation is necessary to inhibit Epac-induced cell migration.
Ectopic differentiation of ABCs may cause a change in cell migration, preventing the normal displacement of the slow fibres by the fast fibres.
The SUM 1315 shRNA results described above demonstrate not only a significant reduction in the amount of TWIST1 expression, but also a phenotypic change in cell migration, suggesting that these shRNA sequences were effective in knocking down TWIST1 expression.
Although the results of the migration analyses may in part be explained by a reduction in cell number rather than a change of cell migration ability, the analysis of mRNA levels confirmed down-regulation of cell motility-associated genes such as MAPK12 [ 42], PLCG2 [ 43] and NCF4 [ 44] in all three FOXP1 transgenic neuroblastoma cell lines analyzed.
Significantly, heregulin-induced intracellular signalling was dramatically reduced in cells in which the expression of CD44 was suppressed (via siRNA), with a corresponding loss of heregulin-induced migratory behaviour (mean fold change in cell migration versus untreated control: 6.7 ± 1.1, P < 0.05 (heregulin beta 1); 1.8 ± 0.9 (CD44 siRNA); 1.47 ± 0.6, P < 0.05 (heregulin beta 1 + CD44 siRNA)).
The wound closure rates, in the presence of anti-PGRMC1 antibody, demonstrated no change on cell migration pattern as compared to those induced by P4 alone or by P4 + PP1 (WC 15.2 ± 6.1% and 10.2 ± 1.4% versus 37.3 ± 3.4%, P values were 0.047 and 0.008, resp .. Treatment of anti-PGRMC1 antibody alone had no effect on cell migration (37.8 ± 4.3% versus 37.3 ± 3.4%, P = 0.93).
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