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Chemokines can attract T cells to the tumor site and tumor intrinsic pathways can influence the composition of local chemokines.
Data described herein indicate that NO, acting through cGMP-independent pathways, can influence the EBV life cycle.
Mutations in important driver genes, arising from various defects in the DNA damage response (DDR) pathways, can influence the tumor response to treatment.
As des-cribed above, other signaling pathways can influence R-Smad (poly- ubiquitination and degradation via CDK8/9- and GSK-3-mediated linker poly- ubiquitination
Here, we demonstrate Syk and CARD9 signaling pathways can influence TLR5-mediated antigen presentation and that Syk and CARD9 expression are required for optimal activation of flagellin-specific CD4+ T cells.
Our data also suggest that combinations of effects across multiple pathways can influence facial shape and the generation of dysmorphology in ways that are complex and not easily predicted.
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For example, numerous studies on complex diseases have demonstrated that genes functioning in the same pathway can influence imaging QTs collectively even when constituent SNPs do not show significant association individually [18].
Many previous pharmacogenetic studies have been focused on genetic variation in genes within this pathway, and there is evidence showing that variation in the expression of genes within this pathway can influence response to cytidine analogues [7], [29], [30].
Studies in mammalian cell lines have shown that the insulin receptor pathway can influence translation of HIF-1α, and recent studies in C. elegans have suggested that DAF-16 might regulate HIF-1 expression in some developmental or environmental contexts [28], [29].
The two pathways are linked, and molecules in one pathway can influence the other [ 102].
The TF pathway can influence inflammation via interactions with PAR1 and PAR2.
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