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Different low levels of cell wall matrix components have a strong impact on the microfibril architecture and enable moisture penetration upon hydration.
A host of soluble factors such as growth factors, chemokines, eicosanoids soluble metabolites and extracellular matrix components have been extensively documented as factors which modulate this environment.
Considering that many of these matrix components have signaling activities associated with regulation of cellular proliferation and migration similar to those described for EMT, the profibrotic phenotype described here may represent a defining component of advanced lung SCC.
The growth characteristics of examined cells on extracellular matrix components have previously been published [ 4].
Importantly, these extracellular matrix components have been linked to lymphocyte adhesion and migration and to islet inflammation [ 32, 69 ].
Again, no specific matrix components have been identified that help to maintain MSCs in their naïve state, as a niche matrix would do.
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This deposition of intratumoral extracellular matrix components has three possible origins: they could be produced by adjacent stromal cells, by normal brain cells that are activated by the invading glioma cells [35] and/or by the tumor cells themselves as part of their mesenchymal differentiation (see below) [36].
The role of these smaller matrix components has been demonstrated to be important in collagen fibrillogenesis [ 19].
Recently, interaction of lignin with other wall matrix components has become a focus of cell wall research [ 13].
In such a context, the identification and characterization of organic matrix components has stimulated numerous studies recently reviewed [ 7, 34].
The ability of tumor cells to interact with the components of the NECM affects numerous cellular processes, and inappropriate expression of these matrix components has been associated with glioma invasion and growth [ 8, 14].
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