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Stimulation with recombinant ephrinA1-Fc led to strong activation and degradation of endogenous EphA2 in PC3 cells (Fig. 1D), consistent with previous observations10.
In 1973, Tim Bliss and Terje Lømo described a phenomenon in the rabbit hippocampus that appeared to meet Hebb's specifications: a change in synaptic responsiveness induced by brief strong activation and lasting for hours or days or longer.
Treatment with only NPRL2 induced strong activation and cleavage of caspase-2, suggesting that the activation of caspase-2 may be one of the early NPRL2-mediated molecular events.
Second, the detection of T-cells bearing endogenous TCR in RAG-deficient Tg mice needs strong activation and selection either by allogeneic stimuli, as in the present study, or autoimmune reactivity [20] that do not often occur in classical protocols using specific immunization.
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Many of the links that lose significance come from the middle cluster, which has little positive or negative correlation, but we also lose most of the links from the clusters with the strongest activation and inhibition signals.
When bioequivalent amounts of P, MPA, DRSP (all 100 nM) or NES (1 nM) were administered to T47-D cells, visible differences in moesin Thr-phosphorylation were seen, with MPA inducing the strongest activation and DRSP the weakest (Fig. 5A).
Signalling through laminin-binding integrins often features minimal activation of RhoA, which controls the formation of actin stress fibres and prominent focal adhesions, and strong activation of Rac1 and Cdc42, which control the formation of lamellipodia and filopodia, respectively.
When an Arabidopsis promoter AtDFR[ 32], fused to luciferase was used, MYB110a showed strong activation with and without AtTT8, while AtMYB75 was significantly stimulated by the presence of AtTT8.
However, overexpression of p38 and ERK1/2 significantly decreased BMP-2-induced Runx2 expression and p6XOSE2-Luciferase activity, indicating that strong activation of p38 and ERK1/2 signaling has a negative role in Runx2 expression and activation.
We found that the cystine-addicted breast cancer cells and tumors have strong activation of TNFα and MEKK4-p38-Noxa pathways that render them susceptible to cystine deprivation-induced necrosis.
As expected, the combinations of cladribine and S3I-201 induced strong activation of caspase-3 and -8, and PARP cleavage in all three MM cell lines.
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