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In diploid cells of the budding yeast, Saccharomyces cerevisiae, growth on low-ammonium solid media stimulates a signal-transduction network [2] mediating a switch from the ovoid single-cell yeast form of growth to a pathogen-like filamentous form characterized by cell elongation, unipolar distal budding to form cell chains, and substrate invasion [3].
The microtubular cytoskeleton may participate mainly in later stages of invadopodia extension or subsequent cell migration rather than the early steps of substrate invasion per se[ 26, 193].
Ste12p is conserved in many fungi, regulating processes involved in mating, filamentation, substrate invasion, cell wall integrity and virulence [ 34], while MADS-box proteins bind to DNA and have dimerization activity [ 35].
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Hakai's influence on cell attachment to the substrate and invasion capacity of epithelial MDCK cells was addressed [ 89].
To investigate this possibility, we studied Hakai's influence on cell attachment to the substrate and invasion capacity of Madin-Darby canine kidney (MDCK) cells.
Moreover, novel human substrates in the nucleus or in the cytoplasm for Hakai need to be identified to clarify its influence on cell phenotype, including cell-substrate and invasion capability in tumor cells.
Our data suggest that Hakai may have an important functional role during oncogenesis through its implication on cell adhesion to the substrate and cell invasion.
In addition, the more recent study from this laboratory showed that TNF- α stimulated and alpha-melanocyte stimulating hormone (α-MSH) opposed cell attachment to ECM substrates and cell invasion through fibronectin, both of which would be consistent with TNF- α promoting metastasis and α-MSH providing partial protection against the action of TNF- α.
Exogenously overexpressed CTSB increased cancer cell invasion and substrate proteolysis, effects that were inhibited by CST3.
In the apical complex, proteins secreted from specialized secretory organelles, microneme and rhoptries, mediate adhesion to the cell substrate during motility and invasion or formation of a PV (Baum et al., 2006).
In contrast, correlation of levels of Neu protein with only proliferation rates and not with substrate adhesion, motility or invasion is consistent with the expression of the neu transgene causing the largely proliferative breast lesions and noninvasive breast tumours observed in transgenic mice (Davies et al, 1996) and rats (Davies et al, 1999).
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