Sentence examples for binding we created a from inspiring English sources

To determine whether one of these two domains in Roc proteins is responsible for specific Cullin binding, we created a series of chimeric constructs that join the NH2-terminus of one Roc protein to the COOH-terminal RING domain of another (RING-swap constructs, Fig. 2A).

To verify whether these SIMs enabled SUMO binding, we created a mutant that lacks all of these motifs, by mutating large hydrophobic residues into alanines (ΔSIM mutant).

To analyze the effect of p.E113K substitution on DDR2 collagen binding, we created a soluble ectodomain construct with the p.E113K mutation and expressed it in HEK293-EBNA cells.

Therefore, to experimentally identify residues in this region of DmsD that permitted signal peptide binding, we created 2 random libraries of DmsD variants using an NNK library approach that targeted residues W72/L75/F76 in the putative binding pocket [43].

To verify the specificity of ER binding sites, we created a heat-map based on previously published ChIP-Seq data [ 21, 45].

In contrast to existing methods based on engineering of DNA-binding proteins, we created a Cas9-based transactivator that is targeted to DNA sequences by guide RNA molecules.

To test requirements and mechanisms to elicit enhanced combination-activity with different EGFR binding domains, we created an anti-EGFR biparatopic antibody.

To identify potential cell surface-localized binding partners of PVRL4, we created a C-terminally HA/FLAG-tagged PVRL4 construct and first verified that cell cell clustering as well as anchorage-independent growth phenotypes were not affected by the addition of a C-terminal tag (not shown).

To eliminate the TR-binding ability of zTERT, we created a mutant harboring a deletion of the entire 587 N-terminal amino acids (ΔTR-zTERT), based on the previously identified TR region of hTERT [6], [12] (Figure 6A).

To determine which aa residues in the gp41 MPER epitope mediate high frequency, low affinity binding to IgMa B cells, we created a series of MPER peptide variants by alanine substitution (Fig. 7A) and compared their binding of gp41 MPER with 2F5 (Fig. 7B, top panel) to binding with BALB/c splenic B cells (Fig. 7B, middle panel).

To finalize this comprehensive verification of the three-step model of TBP binding to a promoter [ 47, 49], we created a freely available Web service [ 62] for users who wish to apply this bioinformatics application to data on the TBP/promoter-complexes in humans: http://beehive.bionet.nsc.ru/cgi-bin/mgs/tatascan/start.pl.