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Whether the increase is caused by increased expression or decreased degradation of γ-crystallin in the heterozygous and homozygous αB-R120G mutant lenses remains to be determined.
In this study, we hypothesize that deregulated glutamatergic synaptic transmission/plasticity, caused by increased expression of GRIN1 and hence increased density of NMDA receptors, may affect neuronal growth in autism by shifting APP processing to the production of sAPP α through ERK-mediated α-secretase activity.
However, this MG132-induced increase in ACh release was presumably caused by increased expression levels of proteins necessary for ACh synthesis/release and was independent from the misfolded SOD1-induced effect (Supplementary Material, Figs S4B and C).
Next, we tested whether L435-3-mediated L435-3-mediated L435-3-mediatedn minhibitionused by increased expressiof of IAVereplication
Further, T-cell responses decline with age due to an age-associated defect in T-cell receptor signaling, which is caused by increased expression of phosphatase 6 and miR-181a.
Cell size is not affected by the suppression of cell death, and remains similar to that caused by increased expression of MAP4K3 (Fig. 3H).
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Reprobing the membrane with a total ERK1/2 antibody indicated that the total ERK1/2 content was not changed, suggesting that the increased ERK1/2 phosphorylation was not caused by increased ERK1/2 expression.
It can be discussed, however, that the deterioration in pulmonary function was probably not solely due to the excessive increase in plasma NOx concentrations caused by increased iNOS expression, because these were later events and the pulmonary oxygenation index was already markedly reduced as early as four hours after the injury.
Therefore, this result indicated that improved upregulation of rOat3 function in T2DM by SNE was not caused by increased Oat3 expression but probably involved with other mechanisms.
DOI: http://dx.doi.org/10.7554/eLife.00996.003 10.7554/eLiFigure96.004 Figure 1 figure supplement 1. Promotion of breast cancer by pregnancy is not caused by increased oncogene expression.
To evaluate whether the dampening of TLR5 mediated IL-8 production by IRAK-M was caused by increased mRNA expression of negative feedback inhibitors such as A20 [ 13] we determined A20, SHIP-1 and SOCS-3 transcript levels in H292 cells that overexpressed WT or mutant IRAK-M proteins after 3 hours of stimulation.
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