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Almost all existing nonlinear optical effects have been observed in dye-doped LC compositions, in which the absorbing dye molecules trigger the LC director reorientation [4].
These results suggest that the early TNF response is mediated by hypoxanthine degradation into uric acid, but that additional inflammatory parasite-derived molecules trigger the late secretion of TNF.
When it is stimulatory, what initiates the change to an inhibitory effect, and which signalling molecules trigger the change are not precisely understood [ 49].
The mechanisms by which small molecules trigger the immune response in plants have been widely studied in the model plant Arabidopsis thaliana, but less is known about the ways in which peptidoglycan fragments can initiate an immune response.
Overall, our data show that Cry toxins are versatile proteins that could exert toxicity by different mechanisms of action and the protoxin molecules trigger the formation of pre-pore structures involved in toxicity.
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In a typical model of NF-κB activation, the recognition of pathogen associated molecules triggers the canonical NF-κB pathway that depends on the phosphorylation of Inhibitor of NF-κB (IκB) by the catalytic subunit IκB kinase β (IKKβ), its degradation and the nuclear translocation of NF-κB dimers.
The release of these pro-inflammatory molecules triggers the recruitment of innate immune cells to the site of infection and elimination of the pathogen.
LPS binds to surface TLR4 molecules, triggering the secretion of various inflammatory factors, which contribute to the pathophysiology of septic shock and other immune disease.
Bid like other BH3-only molecules triggers the release of cytochrome c from mitochondria ultimately resulting in activation of caspase-9 [ 45, 40].
TLRs are expressed on multiple cell types (such as dendritic cells and macrophages) and generally respond to "danger signals" (e.g., pathogens and damage associated molecules) triggering the production of inflammatory cytokines and chemokines.
The ligand-dependent recruitment of these adaptor molecules triggers the activation of multiple signalling pathways, including the JNK, ERK and p38 mitogen-activated protein kinases (MAPK), the transcription factors NF κB, STAT and the phosphatidylinositol 3 kinase (PI3K) cascade, which act in concert to regulate many of the pleiotropic activities of CD40 in a cell type-dependent manner.
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