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The gene YALI0B19382g is associated with three reactions (R0161, R0164, and R0176) in the FAS pathway.
Fas pathway has been investigated as a potential contributor to the inflammation and alveolar epithelial cell apoptosis observed in the lungs of patients with ALI [41, 42].
One potential way to bypass these particular challenges due to the expression of TLR4 on glioma cells is through the activation of the Fas pathway.
These results have important implications for understanding the role of the Fas pathway in pathogenesis of autoimmune diseases and for designing novel FasL-modulating therapies.
The strategies for production of advanced biofuels have converged upon four major metabolic routes: the 2-ketoacid pathway, the fatty acid synthesis (FAS) pathway, the isoprenoid pathway, and the reverse β-oxidation pathway.
This demonstrates for the first time that cisplatin does not signal for death via the fas pathway, but it does initiate the mitochondrial stress pathway in neurons and that NGF blocks death upstream of bax redistribution.
All the genes except for the EC 3.1.2.14 gene were homologous to E. coli genes and were used to improve the enzymatic activities to over-express components of the FAS pathway through metabolic engineering.
The Fas pathway is a major regulator of T cell homeostasis, however, the T cell population that is controlled by the Fas pathway in vivo is poorly defined.
The Fas pathway is involved in osajin-induced apoptosis of NPC cells.
Thus, we hypothesized that avicins may induce cell apoptosis by activation of the Fas pathway.
Thus, we hypothesized that avicins may induce apoptosis by activation of the Fas pathway.
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