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Taken together, these data strongly indicate that the mode of motility employed by neutrophils in interstitial tissues is consistent with a previously described model of amoeboid motility [16], characterized by high speed adhesion-independent movement associated with a low degree of cytoskeletal organization and a lack of discrete focal contacts.
A similar mode of motility is observable for tumor cells during protease-independent migration (Wolf et al., 2003).
For the quantification of the parasites that are changing the mode of motility it is essential to consider that while some parasites are losing straight/fast mode, the numbers of the parasites with curved/slow mode of motility is not increasing.
Because of that we decided to trigger overexpression of the β- or γ-actin isoform in the human colon cancer cell line BE, representing the mesenchymal mode of motility, and to observe its effects on cell migration and invasion capacities.
Irrespective of the complex crosstalk between Rho GTPase family members, which requires further studies, the loss of clonogenic survival and abolishment of VM phenotype caused by loss of BNIP3 in melanoma cells, indicate that rather than affecting a particular mode of motility, BNIP3 modulates essential processes supporting cancer cell survival and spreading.
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We showed here that mutations in fadD genes, important for FA β-oxidation in P. aeruginosa, also influenced two modes of motility and virulence factor expression.
Cancer cells disseminate from primary tumor sites utilizing different modes of motility and invasion, including protease-independent amoeboid crawling, and integrin- and protease-dependent mesenchymal migration [ 5- 7].
Three key factors are affecting the shift between modes of motility: stiffness and composition of ECM (Brabek et al., this issue [ 4]), intratumoral hypoxia [ 7] and the cellular stromal counterpart of the tumor mass (Calorini and Bianchini, this issue, [ 8]).
In this context we would like to note that our data from the trap (like the data from TIRF) shows that the same beads can undergo different modes of motility (i.e., diffusion, processive stepping – see Figure 2E).
The choice of migration styles enables cells to use ad hoc mesenchymal or amoeboid modes of motility and grants to cells of aggressive cancers the ability to move in environments with different structural characteristics using either matrix proteases to degrade the extracellular matrix (ECM) or squeezing between its gaps.
Previous studies have reported that GEF-H1 regulates the interaction of actin and microtubule at the leading edge and focal adhesion turnover [ 47, 48] that are involved in mesenchymal motility [ 49, 50], suggesting the involvement of GEF-H1 in this mode of cellular motility.
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