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For example, genes involved in protein trafficking have recently been identified to be involved in α-synuclein toxicity, leading to the hypothesis that α-synuclein mediated altered intracellular trafficking regulates dopamine homeostasis [5].
Our results thus link expression of VAP(P58S) in neurons to modulation of TOR signalling – a well defined pathway involved in regulating nutrient sensing, cell growth and aging, suggesting that TOR mediated altered cell metabolism might contribute to VAP(P58S) mediated ALS.
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It is likely that other mutations exist and that they may mediate altered enzyme activity in these individuals [32].
In the present study we interrogated this subset of genes and identified a role for the transcription factors CREB and E2F1 in mediating altered actin and cytoskeletal related dynamics.
We next hypothesized that small decreases in β-cell mass mediate altered glucose regulation in settings of borderline glycemic control.
As abnormalities in the actin cytoskeleton are detected early during the course of AD, RanBP9-mediated altered cofilin signaling can lead to the formation of cofilin actin rods, which may attract hyperphosphorylated tau and promote tau pathology followed by synaptic dysfunction.
We identified a Ras-nitric oxide (NO) pathway that mediates altered myelin structure.
Using flow cytometry and gene profiling, we found that CaMKII mediates altered leukocyte infiltration kinetics and pro-inflammatory chemoattractant signaling, indicating that CaMKII regulates pathological post-infarct remodeling via inflammatory pathways rather than via early induction of cell death.
The results of all of our findings taken together indicate that the ability of the LHRH analogue Cetrorelix to alter the adhesive profile of these cells is at least partly mediated through altered EGFR signalling.
The equivalent off-rate of Tr1D3 and Tr4 demonstrated that the change in Tr's biotin-binding stability is not mediated through altered subunit interactions.
Inactivation and eventual elimination of duplicated genes can be mediated by altered epigenetic regulation, deletions, TE insertions, and/or point mutations causing premature stop codons.
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