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These kinases modulate a number of transcription factors including NFκB, AP1 and CREB, each of which regulates a plethora expression of immediate early genes central to the inflammatory response [ 41].
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Since production of specialized metabolites is tightly connected to morphological differentiation and depends on a plethora of environmental conditions, expression of CSRs hinges on a variety of other pleiotropic, higher-level regulators that sense and transmit signals to them.
Nuclear factor kappa B (NF-κB) is a major pro-inflammatory transcription factor controlling the expression of a plethora of genes involved in inflammation and immune responses [60].
The fact that in vivo inhibition of PARP-1 reduced the expression of a plethora of chemokines could partially explain the absence of inflammatory infiltrates in the joint tissues of AIQ-treated mice, being especially relevant for chemokines as MIP-2 (chemotactic for neutrophils) and Rantes (for macrophages and T cells), all involved in CIA pathogenesis [21], [22].
miRNAs modulate both physiological and pathological pathways by post-transcriptionally inhibiting the expression of a plethora of target genes.
The transcription factor NFκB is a crucial regulator of immune and inflammatory responses, controlling the expression of a plethora of genes including cytokine, cytokine receptor, chemokine, cell adhesion molecule, and other cell surface receptor genes [ 42, 43].
Phosphorylation of myocyte-specific enhancer factor 2 (MEF2) and CCAAT-enhancer binding protein (C/EBP β [ 354] has also been reported, thereby triggering the expression of a plethora of genes involved in cell type-specific differentiation.
We now add data that methylation of CpG dinucleotides also may play a key role in controlling expression of a plethora of genes involved in directing tissue specificity and diverse organ function.
Altogether, these results suggest that the hERG1 agonist NS1643 inhibits proliferation of SKBr3 cells by downregulating the expression of a plethora of important cell cycle phase-specific biomarkers including an early decrease of cyclin E2.
The latter, together with NFAT and transcription factors activated by MAP kinases downstream of Syk, regulates the expression of a plethora of innate response genes, including those encoding co-stimulatory molecules and pro-inflammatory cytokines and chemokines 7, 9– 12. Notably, unlike the TLR, Dectin-1 not only regulates gene expression but can also function as a phagocytic receptor 10, 13, 14.
The scope of central tolerance in the thymus is largely dictated by the ectopic expression of a plethora of tissue-restricted antigens (TRAs) by thymic epithelial cells (TECs), in particular medullary thymic epithelial cells (mTECs), a phenomenon termed promiscuous gene expression (pGE).
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