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Hemolysin is known to be required for cellular invasion and cytotoxicity [22]; hemolysin-negative E. tarda mutants could not invade human epithelial cell lines [36].
Under these circumstances, TERT may be able to alternatively function in cellular proliferation and mobilization, or may be required for cellular differentiation and survival independent of telomere metabolisms.
Collectively, these data suggest that the physical presence of FAK or the signal transduction associated with FAK does not seem to be required for cellular proliferation in human endothelial cells.
The S. pombe has provided a powerful model system for investigating the chromosomally borne epigenetic mechanism of asymmetric cell division, which might be required for cellular differentiation in higher organisms as well.
Although Rho GTPases have been shown to be required for cellular functions associated with tumour progression and invasiveness (Schmitz et al, 2000; Price and Collard, 2001), studies supporting the role of Rho for carcinogenesis and tumour progression in patients with cancer are largely missing.
In contrast with the paradigm of the inverse regulation of cell growth and autophagy by TOR signaling, autophagy has been shown to be required for cellular overgrowth driven by the evolutionarily conserved transcription factor Myc. Myc is required for autophagy, both in Drosophila and mammalian cells [ 73, 132].
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The GARP complex is required for cellular sphingolipid homeostasis.
The SNX5/6 IncE interaction is required for cellular localization of IncE and its inhibitory function.
Regulation of protein interaction domains is required for cellular signaling dynamics.
Efficient patterning of large areas with nanometre features is required for cellular engineering applications.
Bromberg, J. F., Horvath, C. M., Besser, D., Lathem, W. W. & Darnell, J. E. Jr. Stat3 activation is required for cellular transformation by v-src.
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