Sentence examples for binding site was deleted from inspiring English sources

The same procedure was used to clone Luc-VEGF-A-UTR and Luc-VEGF-A-UTR-d where the putative miR-205 binding site was deleted.

Next, the wild-type (WT) constructs containing let-7a binding CCR7 3'UTR and mutant type (MUT) constructs were prepared, in which the binding site was deleted.

In the whole-site deletion variant, the entire 22 bp sequencing corresponding to the length of miR-503 at its binding site was deleted (QuikChange Lightning Mutagenesis Kit, Agilent).

An intronic sequence of 238 base pairs including a putative GATA binding site was deleted by partial digestion of the full-length plasmid with ScaI, followed by HindIII digestion, Klenow reaction to fill in the protruding ends and blunt-end recircularization.

First, seven nucleotides of the nine-nucleotide sequence in the BP1 binding site were deleted to generate delLB170, followed by insertion of the mutated sequence, described in [ 23], to create mutLB170.

If the Pho4 binding sites are changed in a variant, the labels b and c occur on different edges of the wild-type graph, while if a Pho4 binding site is deleted, some vertices become inaccessible and the graph changes from the 12-vertex wild-type graph to a graph with eight vertices.

Coupling of linear porphyrin dimer P2 in the presence of the regular D6 h T6 template gives the cyclic hexamer c- P6.[ 3b, d] If two adjacent pyridine binding sites of the T6 template are deleted to give T4, then the main product becomes the cyclic octamer c- P8, or if only one binding site is deleted, the main product is the cyclic decamer c- P10.

When one of the two potential RUNX1 binding sites was deleted, basal luminescence intensity and induced luciferase activity after RUNX1 and/or CBF β transfection were abolished.

For generating mut-hTRIM32-luc promoter plasmid, the region spanning from −367 to −59, containing the putative p73-binding site, was deleted.

Moreover, transfection with the shortPRO-MyoDluc vector in which the MyoD-binding site was deleted resulted in a 2.7-fold reduction in luciferase activity as compared with the WT construct, demonstrating that the Ankrd2 promoter is positively regulated by MyoD.

In contrast, stimulation with neither VEGF nor Elk-1 overexpression increased miR-17 92 miR-17 92activity when the Elk-1-binding site was deleted from the promoter reporter construct.