Sentence examples for binding was abolished when from inspiring English sources

Consistent with ChIP, in vitro DNA binding assay showed that purified MAF1 protein could indeed bind to the CDKN1A promoter that contained the MIR3 element, but the binding was abolished when the MIR3 repeat element was deleted, which indicates specificity of MAF1 binding to the MIR3 element.

PABPC1 binding was abolished when all three regions were deleted (i.e. PAM2, M2 and C-term; Figure 2C, lane 19; Zekri et al, 2009).

This specific binding was abolished when B-CK was pre-treated with an irreversible I2 ligand, BU99006, further indicating the existence of an I2 binding domain in this enzyme.

Indeed, enhanced binding of TBP was observed at the CDKN1A promoter after MAF1 knockdown, and the binding was abolished when there was simultaneous knockdown of Pol III and MAF1.

Competition experiments with unlabeled probes containing mutations of conserved nucleotides showed that Zfp335 binding was abolished when both DNA elements of the bipartite motif were mutated, whereas mutations in either the first or second element had an intermediate effect, indicating that both parts of the consensus motif are required for full Zfp335 binding.

This suggests that in the absence of the CB and CD sequences, repressive factors bind to the modified promoter, and that this binding is abolished when either CA or CC are removed in addition.

Figure  4 shows that the highly conserved adenosine residues in the motif are critical as GlnR binding is abolished when these residues are mutated.

This study has added to our understanding of MeCP2 function by discovering that the basic cluster flanking R306 has an additional function in binding DNA and that this binding is abolished when basic residues in the cluster are mutated to neutral or acidic residues.

However, in the absence of Ser37, stimulating cells with the adenylate cyclase activator forskolin caused a marked increase in 14-3-3 14-3-3 14-3-3M122A, which was abindingd when Ser62 was also mutoted to alanine and when cells were pre-treated with H89, which is a non-speciFAM122AP-dependent protein kinase (PKA) inhibitor (Fig. 2D).

Interestingly, the tendency of isolated hcTnCL29Q to induce a significant change of Ca2+ binding to the regulatory site was abolished when hcTnCL29Q was incorporated into regulated thin filaments [ 15].

This inhibition response was abolished when miR-29 binding site was mutated, since this mutation (pLuc-3URTmutant-p85) prevents miR-29 binding to targets in the mRNA.