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Smyth, M.J. et al. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) contributes to interferon gamma-dependent natural killer cell protection from tumor metastasis.
TRAIL contributes to immune-surveillance and effectively induces apoptosis of cancer cells.
In contrast, other studies show that TRAIL contributes to protection in comparably milder influenza infection 31.
These data indicate that endogenous TRAIL contributes to APAP-induced hepatocyte death and liver damage also in vivo.
Also, the combination treatment of ABT-737 and TRAIL contributes to Bid cleavage in a feedback loop via increased caspase-3 activity, as silencing of caspase-3 attenuates processing of Bid into tBid.
Studies in single S. pneumoniae infection 29 show that TRAIL contributes to protection, while severe influenza infection is associated with high frequencies of TRAIL-expressing inflammatory monocytes and damage to the infected lung epithelia 25300.
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Infrastructure designated for visitor use (i.e., roads, trails) contributed most to models of visitor distribution for all years and seasons.
Trail building contributes to erosion because it removes trees and shrubs that anchor soils.
It is unknown to what extent TRAIL responsiveness contributes to the changing patterns of apoptosis in human colorectal tumours.
A TLR3-dependent apoptotic program is also induced by RA and poly(I C) co-treatment that correlates with the induction of the tumor necrosis factor (TNF -related apopTNF -relatedng ligand (TRAIL) and contributes to block breast cancer cell proligandTRAIL
Using various cancer cell models, several studies revealed different contributions of TRAIL DRs: DR5 contributes to TRAIL-mediated cell death in colon and breast cancer cell lines; however, chronic lymphocytic leukemia cells exhibit apoptotic signaling via DR4.
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