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However, we cannot exclude the involvement of additional signaling pathways also leading to NF-κB activation, nor can we exclude the possibility that MyD88-independent induction of colonic SAA3 expression could be due to downstream pathways other than those involving NF-κB (i.e., MAPK and PI3K pathways).
Part of that explanation appears to be due to downstream signaling [116].
This increase may be due to downstream effects on Aβ plaque dissolution.
Thus, it is possible that many of the cellular and molecular effects observed in curcumin treated cells might be due to downstream effects rather than direct interactions with curcumin.
COX-mediated neuronal injury is thought to be due to downstream effects of one or more prostaglandin (PG) products, including PGE2, PGD2, PGF2α, PGI2 and thromboxanes (particularly TXA2) that effect cellular changes through activation of specific prostaglandin receptor subtypes and second messenger systems [ 69, 76, 78].
On the contrary, purifying selection was found to act more severely on genes acting at the downstream part of the network, which seems to be due to downstream genes being more highly and broadly expressed, having certain functions and, in particular, encoding proteins that are more highly connected in the protein protein interaction network.
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Control experiments indicate that the antibacterial effect of sNAG is not due to a direct interaction of the material with the bacteria but is due to downstream affects such as the regulation of defensins by Akt1 activation.
Intra-VTA AM251 significantly increased Fos-IR in several hypothalamic nuclei, including DMH and VMH, which was not observed with peripheral AM251, suggesting that cellular activation within these regions was due to downstream activation of the VTA.
This is due to downstream information, as in the total concentration of pSTAT5, i.e. the observable y1, this plateau is also present with some delay.
Additionally, it may be assumed that T cells may bear ET-1 receptors on their membrane and that the changes of LFA-1 and L-selectin expression we detected in our patients with SSc-PAH are due to downstream signals following direct stimulation by ET-1, subsequently inhibited by bosentan.
Is it possible that BRCA1-dependent ubiquitination at DNA damage foci may be due to a downstream un-identified E3 ligase?
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