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In line with our observation, activation of p38 with preconditioning stimuli or over-expression of MKK3/MKK6 has been reported to protect the heart against myocardial I/R injury [ 53- 58].
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Such an integrative function is consistent with our observation that activation of these cells produces persistent behavioral effects, as persistent activity is a hallmark of neural integrators (Major and Tank, 2004; Goldman et al., 2007).
The apparent salutary effect of these drugs was followed by the observation that activation of the mTOR pathway may be a predictor of poor prognosis [15], [16].
Double labeling of irradiated iPS cells with NANOG and TP53-serine 15 validated observation regarding activation of checkpoint signaling in pluripotent cells.
This is based on the observation that activation of an oncogene is followed by a burst of hyperproliferation that results in replicational stress, DDR activation and ultimately senescence.
Moreover, this underlines the observation that activation of the RAS/RAF kinase pathway by increased expression levels may cause biological effects different from that of activation by mutations.
This possibility is supported by the observation that activation of Wnt signaling in axin1 mutants phenocopies parapineal ablation with respect to neurons bilaterally adopting dHbm identity.
The observation that activation of the C-type gate renders the channels resistant to ML67-33 whereas loss of coupling to Ct does not affect ML67-33 actindicatesndicathatthat ML67-33 acts directly on the components comprising the C-type gate.
Our observation that activation of Myosin II, which regulates Filamentous actin (F-actin) contractility without affecting F-actin levels, cooperates with RasACT to promote JNK activation and tumorigenesis, suggests that increased cell contractility is a key factor in tumorigenesis.
A first line of evidence was provided by our observation that activation of CG genes in melanoma cells correlates with the presence of a gene expression signature that has been previously associated with DNMT1 depletion [ 28].
Recent data in invasive breast cancer support the observation that activation of the PI3K pathway or loss of phosphatase and tensin homolog (PTEN) is associated with resistance to trastuzumab [ 25, 26].
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