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When CC2D1A was bound to PDE4D5 the activity was not affected by PKA suggesting that CC2D1A-binding PDE4D may prevent activation by PKA phosphorylation.
As SOX7 decreased Wnt/β-catenin-stimulated transcription [42], it is possible that the inability to suppress the constitutively expressed SOX7, which may prevent activation of β-catenin via Wnt3a signaling, is responsible for the absence of PS/ME/DE induction.
Interestingly, we observed that sexual genes have more densely nucleosome-packed promoters that may prevent activation of these genes during the asexual cell cycle.
On the contrary, a high proportion of FOXP3+CD25high T cells this early in life may prevent activation and necessary maturation of the immune system, thereby favouring faulty programming that may lead to sensitization in children.
Ligand-targeting compounds, or co-inhibition of the IGF and HIF-1 systems, may prevent activation of compensatory signalling, thereby providing a valuable addition to IGF-1R inhibitor-based therapies.
Furthermore, at sufficient concentrations, soluble native CRP may prevent activation of the classical complement pathway on biological surfaces due to consumption of soluble C1q without binding C2/C4 [ 14].
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In addition, cleavage and subsequent degradation of the E-cadherin cytoplasmic tail may directly prevent activation of signaling cascades that depend on the recruitment of cytoplasmic effectors, such as phospatidylinositol-3 kinase, to the E-cadherin tail.
Nevertheless, the use of citrate may also prevent activation of complement by blood-membrane contact and endothelial release of MPO, as seen during heparin anticoagulation [ 16].
Further, decreases in pyruvate-phosphate dikinase activity may prevent possible activation of alternative gluconeogenic pathways, such as that reportedly observed in Rhizobium (Sinorhizobium) meliloti[ 30].
Alternatively, it can be hypothesized that Treg cell suppression of HIV-1-specific T cells, rather than the presence of such responses, may prevent immune activation and susceptibility to HIV transmission.
The mutation may prevent the activation of the RNA transcript (removal of the secondary structure) and hence decrease rpoS translation.
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