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It suggested that miR-200b might inhibit expression of vimentin through TGF- β1-SMAD2 signal pathway.
Alternatively, AhR activation might inhibit expression of FLIP, which is partly controlled by NF- κB, or regulate other target genes that remain to be characterised.
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In proliferating myoblasts, MyoD is associated with histone deacetylases (HDACs), the histone methyltransferase Suv39h1 and heterochromatin protein HP1, and might actively inhibit expression of its target genes by inducing a local repressive chromatin structure [24], [28], [29].
It is known that Srebf2 overexpression induces all 12 enzymes in the cholesterol biosynthesis pathway and inhibition of Srebf2 by TSA might inhibit the expression of these enzymes [ 30].
This implies that insulin might inhibit the expression of ubiquitin E3 ligases through inhibition of AMPK.
Therefore, it is possible that SK1/S1P/S1PR2 signalling might inhibit Brms1 expression through activation of NF-κB, and conversely, inhibition of SK1/S1P induces Brms1 via alterations of p65/RelA phosphorylation.
These data suggested that a potential regulation of miR-98 by RKIP and RKIP might inhibit HMGA2 expression via miR-98 signaling.
Therefore, hypermethylation at the P3 site might inhibit the expression of the NAT, which in turn negatively affects SIP1 translation.
These up-regulated miRNAs might inhibit gene expression of their target genes; therefore down-regulation of these target genes might help the host to inhibit virus replication.
In our results, it is worth noting that cigarette smoking might inhibit nm23-H1 expression and relate to poor survival for OSCC patients at the early T stage by univariate analysis.
Once assembled into an RNA-induced silencing complex, each miRNA might inhibit the expression of hundreds of target messenger RNAs (mRNAs), by inducing translational repression and/or mRNA degradation (1).
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