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Diacylglycerol (DAG), a second messenger generated by phospholipase Cγ1 activity upon engagement of a T-cell receptor, triggers several signaling cascades that play important roles in T cell development and function.
PA-dependent translation activation occurs through the lipid messenger generated by PLD1 directly on mTOR (49 52, 55 58).
Carbon monoxide (CO), an endogenous messenger generated by heme oxygenase-1 (HO-1) [1], has cytoprotective [2], [3], anti-proliferative [4] [6], and anti-inflammatory effects [7] [10] that indicate a potential for clinical applications.
Phosphatidylinositol3-kinases are a family of enzymes that phosphorylate phosphatidylinositol. Phosphatidylinositol 3,4,5-triphosphate is a messenger generated by PI3K, which activates Akt.
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Cyclic nucleotides are second messengers generated by cyclase enzymes from precursor triphosphates and hydrolysed by phosphodiesterases.
This unique gene, localized in B4 band of mouse chromosome 10, is well conserved in mammals and displays 5 different messengers generated by alternative splicing which is one of the main process for differential expression in mammals [ 21- 23].
Therefore, our data are consistent with a model in which Akt translocates to the plasma membrane through the binding of its PH domain to the second messenger PtdIns 3,4,5 P3 generated by PI3K which is activated through Gi/o-protein dependent signaling pathway.
To determine the role of the second messenger ceramide, generated by sphingomyelin breakdown, the intestinal epithelial cell line Caco-2 and primary intestinal fibroblasts from patients with ulcerative colitis or healthy controls were challenged with exogenous SMase or the inflammatory cytokines IL-1β and TNF to induce ceramide generation.
Various studies have demonstrated that not only reactive oxygen species (ROS) per se, but also their oxidation products and other secondary messenger molecules generated by ROS can trigger the programmed cell death [ 5].
When large numbers of phosphorylated messenger proteins are generated by increasing concentrations of extracellular ligands, we demonstrate they generate a self-screening environment that regionally attenuates the cytoplasmic field, slowing movement but permitting greater cross talk among pathways.
PTEN exerts an effect as a tumour suppressor by dephosphorylating the plasma membrane lipid second messenger PIP-3 generated by the action of PI3KCA.
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