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Baculovirus are non-replicative in mammalian cells, but they have been reported to trigger an innate immune response.
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DENV has been reported to trigger a robust type I IFN response; however, IFN-α/β profile in the progression of disease is not well characterized.
During the last decade, FasL has been reported to trigger a RIP-dependent alternative form of cell death, exhibiting necrotic rather than apoptotic features [15].
Moreover, CD64 engagement by immunoglobulins has been reported to trigger a negative regulatory signal that suppresses HIV-1 replication in macrophages.
Carboxylic acid groups have been reported to trigger a dipolar interaction with carbon dioxide.
Depletion of DHODH is reported to trigger a p53 response because of the deficiency in pyrimidine [ 13].
Recently, metalloproteinase-cleaved CD95L was reported to trigger a motility-inducing signaling complex formation in triple-negative breast cancer cells.
Silicone has been reported to trigger a variety of inflammatory and immunological (both humoral and cellular) responses in humans [ 39- 42] and experimental animals [ 43].
Moreover, influenza infection was reported to trigger a generalized stress response, leading to a sustained increase in serum GC level and a systemic suppression of host immune responses [ 21].
Recently, the polyphenol kaempferol has been reported to trigger a ROS-dependent and caspase-dependent cell death in HeLa cells and these cells activate autophagy as a survival mechanism to the drug-induced bioenergetics failure.
Low concentrations of BPA have been reported to trigger a nongenomic proliferative effect in the pancreatic islet, endothelium, breast, and pituitary gland by initiating rapid responses (Bulayeva and Watson 2004; Wetherill et al. 2007).
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CEO of Professional Science Editing for Scientists @ prosciediting.com