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In order to target the DEGs which may cause functional changes, we screened DEGs whose GO terms were closely related with the functions of CIK cells.
To identify such putative compensatory viral changes, we screened a panel of point mutants in the NPC1-binding site of EBOV GP by ELISA for enhanced binders to EhNPC1 domain C.
Based on the assumption that heterogeneity of the cells may be driven by epigenetic changes, we screened promoter methylation of 96 candidate genes in parental breast cancer cells and putative breast CSC using Epitect Methyl qPCR Arrays (results are summarized in Figure 9).
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To investigate the neurochemical properties of the neurons implicated in triggering SP-mediated postcopulatory changes, we behaviorally screened neurotransmitter Gal4 lines driving mSP.
Their foundation also lent the biggest changes we see on screen.
To elucidate the nature of these protein changes, we performed a screening for possible posttranslational modifications (PTM) on the MS/MS level and used a phosphoprotein stain (Pro-Q-Diamond® = Invitrogen, Karlsruhe, Germany) after 2-DE.
On the basis of the knowledge of different stages of behavioural changes we assume that our screening questions make people prepared for such changes.
By directly visualizing morphological changes of infected J774 macrophages, we screened an arrayed F. novicida library of more than 3000 mutants containing two allelic mutations of most non-essential genes [2].
We screened for changes in Ptbx-2:: gfp expression in animals where 724 of the 924 predicted transcription factor genes were individually knocked down.
In this study, we screened for changes in the expression of core promoter factors including TAFs, general transcript factors (GTFs), and mediator subunits (MEDs) upon neuronal differentiation.
By using qPCR, we screened for changes in the levels of pre-ribosome-bound snoRNAs on depletion of each of the putative RNA helicases involved in 40S biogenesis.
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