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Tumor cell survival could also be enhanced through activation of anti-apoptotic pathways such as the PI3K/AKT cascade [39], [40] and Bcl2 and Bcl-xL transcription factors [41].
Although MCF-7/6, MCF-7/Her2.1, and MCF-7/CXCR4 breast cancer cells acquire their malignant phenotypes through different mechanisms and approaches, their invasive potential may be enhanced through activation of a common intracellular signaling pathway that plays an essential role in regulating cancer cell invasion and metastasis.
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As a result of intracellular Ca2+ flux in these settings, deimination or citrullination of arginine is enhanced through activation of the peptidyl arginine deiminase enzymes [ 11].
The synaptic efficacy could be enhanced through both activation of silent synapses and strengthening of already active synapses.
Direct killing of tumour cells occurs through the function of CD8 T cells, but the killing may be enhanced through the activation of CD4 T cells (Hsieh et al, 1993).
The adsorption capacity of such biomaterials can be enhanced through physical or chemical activation.
Generally, in chemically synthesized PEDOT/Au composites, electrocatalytic performances of the composite could be enhanced through Au S thiophene) interactions and the activation of metal ion coordination [27, 28].
The PI3K pathway activation can be enhanced through mutation of PIK3CA or AKT, loss of PTEN or amplification of receptor tyrosine kinases, such as HER2 [3], all of which can contribute to tumour progression.
Tumour cell-selective activation of apoptosis by recombinant human TNF-related apoptosis-inducing ligand (rhTRAIL) is enhanced through co-activation of p53 by chemotherapeutic drugs.
Specifically, cardiac thin filament activation was enhanced through adenovirus-mediated over-expression of a cardiac troponin C (cTnC) variant designed to have increased Ca2 + binding affinity conferred by single amino acid substitution (L48Q).
Adherence is enhanced through consistent adherence support.
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