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The indirect activation of the actin polymerization machinery in mammalian cells by Abp1 via N-WASP might – from an evolutionary point of view – represent an improvement, because N-WASP is a multidomain protein whose activity can be modulated through a variety of signaling pathways [10] [11] and this significantly extends the possibilities for fine-control of actin filament nucleation.
The chromatin condensation status can be modulated through a variety of mechanisms, including post translational covalent modifications of histone tails and recruitment of repressive factors on methylated DNA [ 2].
Alternatively, the interaction could be modulated through a post-translational modification of Six4, as we have previously observed for the association between Ash2L1/MLL2 KMT2B) and phosphorylated Mef2d (Rampalli et al, 2007).
Context can be kept constant in a trial to determine efficacy and can be modulated through a variety of factors in the clinical setting, such as the belief of providers and patients [ 28], attitude and demeanor of the doctor [ 29, 30], enthusiasm for the delivery of the intervention [ 31, 32], cultural contexts and concomitant suggestions regarding diet and health [ 33, 34].
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AMPAR trafficking is modulated through a combination of receptor phosphorylation, ubiquitination, endocytosis, and recycling, yet the factors that mediate these processes are just beginning to be uncovered.
The σ1R activity is modulated through a series of endogenous and exogenous substances.
They suggested that TSA and Kdm4d have no synergic effect because their effects are modulated through a similar pathway.
The activity of VEGFR-3 is modulated through a variety of mechanisms, including its association with VEGFR-2 and alpha 5 integrin [ 64, 65].
The observed HMGA2-induced apoptosis is modulated through a mechanism apparently distinct from that identified in an earlier study, which showed that HMGA1, the other member of HMGA family, induced apoptosis through up-regulation of CyclinA [ 36].
These data indicate that HO-1 expression was regulated mainly by NO generated endogenously in the solid tumour tissue, whereas HSP70 expression was modulated through a separate mechanism, possibly dependent on a hypoxic cellular signalling pathway of the tumour cells.
Using a similar approach to Kendall et al. in which the expression of NRAGE was modulated through a series of loss of function and gain of function experiments, we have found that NRAGE is also a required component in driving NF-κB activation through the BMPR1a-XIAP-Tak1-Tab1 cellsex in 293HEK cells.
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