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Functional analysis of conditional caspase-deficient mice demonstrates caspase-dependent extensive cellular responses such as cell differentiation, proliferation and nuclear factor- κB activation.
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So, active synthesis of Clp proteases, chaperones and antioxidants suggest an extensive cellular response mechanism in Cyanothece ATCC51142 to deal with production of reactive oxygen species (ROS) and protein degradation during photosynthesis and N2-fixation.
Transcriptome and miRNome analysis identified extensive FGF2-regulated cellularesponseses that were both independent and dependent on miRNAs.
We have shown that tumor growth induced an extensive cellular immune response of predominantly regulatory T cells with a presumably protumoral activity.
Thus more extensive analysis of cellular responses is required to precisely determine the inflammatory cell targets for individual CMPs.
Activated Ras signals coming from the plasma membrane are carried over the intracellular compartments by a variety of molecular mediators before reaching their target in the nucleus, where they ultimately control the activity of transcription factors that effectively govern an extensive array of cellular responses.
We hypothesize that acute and persistent infection of professional immune cells (T-cells, monocytes and macrophages) and non-immune cells (endothelial cells and smooth muscle cells) contributes to a sustained inflammatory response mediated by extensive cellular 'crosstalk' and numerous cytokines/chemokines.
In both apoptosis and autophagy, the degraded cells are disposed by phagocytosis without an inflammatory response, in contrast to the extensive cellular disintegration and subsequent inflammation that occur in necrosis.
Topography is one of important ECM physical characteristics that alter the cellular responses in vivo, since ECM topography is responsible for the activation of intricate networks of signaling pathways through extensive transmembrane receptor (i.e., integrins).
Furthermore, free histones in circulation mediate extensive cellular damage, hemostatic imbalance and amplification of the inflammatory response by inducing cytokine production as reported in an animal model of sepsis.
Extensive studies of cdc13-1 mutant cells have generated much insight into cellular responses to telomere uncapping and DSBs.
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