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Specific target binding was demonstrated with self-blocking experiments.
The primary antibody binding was demonstrated with standard avidin biotin-peroxidase complex technique (vector pk-7200).
On fresh cells growing on a Lab-Tek chamber slide (Nalge Nunc Int, Naperville, IL, USA), after nuclear staining with propidium iodide, Sc-284 and C-1801 binding was demonstrated with the appropriate FITC-conjugated Ab.
Similar(56)
Selective binding was demonstrated by turbidity assays with Ricinus Communis Agglutinin (RCA120) lectin.
However, in a chromatin immuno-precipitation (ChIP) study preformed by Scherf and colleagues [24] using anti-pfsir2 antibodies, pfsir2 binding was demonstrated to occur in telomeric regions with repression of upsB expression while it was also clearly shown to not bind or have a direct effect on upsC var genes (upsA genes were not studied).
Increased C-DED binding was demonstrated in the brain of patients with Creutzfeldt-Jacob disease [ 67].
Direct binding of BI6727 to DAPK was demonstrated with the TNP-ATP displacement assay (Supplementary information, Figure S1O).
The binding of the primary antibody was demonstrated with a biotinylated secondary antibody, horseradish peroxidase (HRP -conjugated streptavidin (Dako), and diamino-benzidine (DAB) as tHRP -conjugated
Compared with RRASWT, aberrant binding behaviour of the two RRAS mutants was demonstrated, with RRASG39dup exhibiting an increased binding affinity towards PIK3CA, RAF1, PLCE1 and RASSF5, and RRASV55M to RALGDS.
With the higher dose of RTI-78 at 200 nM, dose-related specific irreversible binding (85%99%%) is demonstrated with increasing radiation dose from 1 cGy to 211 cGy.
A pilot study of 96-plex fsPAG-EMSAs for the Vc2 c-di-GMP riboswitch aptamer binding reactions were demonstrated with linearity observed in a ligand concentration titration study.
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