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Although this orientation-dependent activation hypothesis for single transmembrane receptors was initially debated because of the suggestion that other properties of this EPO mimetic could result in loss of activity [ 40], subsequent studies supported that activation of single transmembrane receptors might be beyond a ligand-induced encounter of the cytoplasmic domains.
Overall, high-content imaging and gene expression data supported that activation of AHR has a stimulatory effect on growth of rHpSCs and loss of viability of rHBs.
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These results provide molecular mechanisms supporting that activation of ex-NMDAR alone is not sufficient to cause death.
Moreover, active Akt in 28% of our tumours, correlated with recurrence and poor patients' survival, supporting that activation of this pathway contributes to tumour growth and therefore to trastuzumab resistance.
Our results support that activation of CB2 receptors increases bone formation by inducing BM-MSCs differentiation.
Further, spinal increases in c-fos after repeated acid injection are prevented by NT-3 overexpression [ 8], further supporting that initial activation of muscle afferents drives central changes.
However, selective inhibition of each pathway supported that the activation of PI3K/AKT, but not ERK1/2, provides survival advantage to the neural progenitor cells.
Evidence supports that macrophage activation and accumulation is one of the major causes for the development of diabetic complications [ 20, 21].
This finding along with the proposed by GO analysis modification of glutathione transferase activity (Table 1) support that activation of detoxifying enzymes might also contribute to cancer chemoprevention by mastic oil in agreement with previous studies indicating the anti-oxidative potential of mastic oil [ 11, 46].
Further support that activation of PERK can strongly inhibit acini formation was obtained by activating PERK signaling in MCF10A cells stably expressing an Fv2E-ΔNPERK construct (Fv2E-PERK) [43].
The above data from animal studies (20, 22) support that activation of the GLP-1 receptor may increase β-cell mass.
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