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This Met degradation might prevent cell protection triggered by ligand-dependent activation of Met.
As previously suggested [ 37], prebiotic oligosaccharides might prevent cell activation and therefore the induction of inflammatory responses by mimicking binding sites on immune cell surfaces.
Another recently uncovered potential mechanism by which RB might prevent cell death is the increased production of reactive oxygen species (ROS) in RB-deficient cells, which leads to autophagy in cells that are also deficient for the tumor suppressor tuberous sclerosis 2 (TSChicashicas et al., 2010; Ciavarra and Zacksenhaus, 2010; Ciavarra and Zacksenhaus, 2011).
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Loss of function, for example, might prevent cells from leaving the cell cycle.
The 129/SvJ allele of Ly49I expressed in CD94-deficient and CD94Tg/– mice binds the MCMV m157 glycoprotein and might prevent NK cell responses to MCMV-infected cells [6].
SMAR1 also inhibited the expression of Fibronectin, Vinculin and JAM2 that are involved in promoting cell-extracellular matrix adhesion, cell spreading and migration [42] [48], suggesting that SMAR1 might prevent tumor cell metastases through negative regulation of these proteins.
It has been speculated that this might be a strategy of the virus to escape the most efficient CTL responses, which are directed against epitopes presented on HLA-A and HLA-B, whereas the lack of down-regulation of HLA-C might prevent the cell from NK-directed killing [51].
By increasing production of those genes, the researchers thought, they might be able to prevent cell division altogether.
Therefore, an increase of the serum hepcidin-25 level in patients with metastatic RCC might prevent tumor cells from utilizing iron by upregulating tumor cell hepcidin as an anticancer mechanism, as well as showing antimicrobial activity if infection occures.
We thus concluded that LL-37 might bind to monosaccharides to prevent cell adhesion of C. albicans (Fig. 5C).
However, combination treatments that allow the use of lower nontoxic doses and/or prevent cell resistance might still offer opportunities for TNF in the treatment of cancer (Wajant et al, 2000; Schotte et al, 2001).
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