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We took an unbiased approach to identify p53-independent pathways activated by defects in ribosome synthesis by analyzing global gene expression in various cellular models of DBA.
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The inert basal surfaces of 2H-MoS2 halsoalso been successfully activated by creating defect sites and/or inducing strain [42 47].
The D band is associated with the breathing modes of the sp2 atoms and is activated by a defect.
The D peak at ~1350 cm−1 corresponds to the breathing mode of sp2 hexagonal carbon but only gets activated by a defect with the help of a double resonance in the inter-valley scattering [26].
To identify p53-independent pathways activated by a RP defect, we used three TF1 cell lines expressing shRNAs against RPS19, RPL5 or RPL11, the three most frequently mutated DBA genes.
However, this ratio may be activated by various types of defects and in a completely independent manner.
They are further activated by oxidative stress or defects of antioxidative defence [ 31– 34], which thus trigger Ca2+ entry and eryptosis [ 5, 28].
It is the result of a two-phonon lattice vibrational process, but unlike the D band, it does not need to be activated by proximity to a defect.
For example, the junction between the aptamer and the Group I ribozyme in the aptazyme Th2P6 resembled the deletion variant td ΔP6-6; the aptazyme was activated by theophylline, while the splicing defect of the deletion variant at 3 mM magnesium was suppressed by 8 mM magnesium or by stabilization of a tetraloop sequence that capped the P6 helix [ 15].
The suspension of ZnO nanoparticles with defects can be activated by both UV and visible light and produce electron-hole pairs (e−h+).
Activated by unattached kinetochores or other spindle defects, the spindle checkpoint response promotes the association of BUB1B, BUB3 and MAD2L1 with CDC20 to form the mitotic checkpoint complex (MCC), which inhibits CDC20 activity.
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